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Biomedical subjects

G Fragasso

Publications and source records attributed to G Fragasso.

At least 55 records · Page 3Linked to original sources
PubMed1994

Reverse redistribution of thallium-201 heralding the development of myocardial infarction: description of two cases.

Development of a perfusion defect on the 201Tl image from exercise to redistribution is referred to as reverse redistribution, a finding which has been previously associated with several conditions. We describe here two cases in which the reverse-redistribution phenomenon, observed in a routine stress-redistribution thallium-201 scan performed because of chest pain, was considered to be artifactual. Both patients subsequently developed a myocardial infarction in the areas showing the delayed perfusion defect. The potential clinical significance of the reverse-redistribution phenomenon in these two cases is discussed. When observed in patients with typical anginal pain, the reverse redistribution pattern should be considered a potential marker of tissue at risk in a region with previous, otherwise undetected, subendocardial infarction. In such patients the need for coronary angiography should be carefully considered.

Adult↗
PubMed1993

Time dependence of residual tissue viability after myocardial infarction assessed by [18F]fluorodeoxyglucose and positron emission tomography.

Areas of myocardial infarction may retain glycolytic activity and this finding is indicative of tissue viability and predictive of functional recovery after revascularization. In order to assess the relation between the time elapsed from the occurrence of acute myocardial infarction and persistence of myocardial metabolic activity in the infarcted tissue, we prospectively studied 65 patients with previous myocardial infarction diagnosed clinically and by electrocardiographic (Q wave) and enzymatic criteria. All patients underwent coronary angiography and contrast left ventriculography, evaluation of regional myocardial glucose metabolism (in the fasting state) by positron emission tomography (PET) with 2-[18F]fluoro-2-deoxy-D-glucose ([18F]FDG), and assessment of myocardial perfusion by single photon emission computed tomography (SPECT) with technetium-99m methoxyisobutyl isonitrile (99mTc-MIBI). Based on the regional metabolic and perfusion findings, patients were divided into 2 groups, depending on the absence (group 1, 26 patients) or presence (group 2, 39 patients) of [18F]FDG uptake in the underperfused regions. Areas of underperfusion at rest, consistent with the clinically identified myocardial infarction site, were observed in all patients. Severity of coronary artery disease, presence of collaterals, number of hypocontractile segments, and wall motion score did not differ significantly in the 2 groups. The time elapsed from the infarction was significantly greater (1,860 +/- 1,333 days) in group 1 than in group 2 (92 +/- 115 days; p < 0.0001). Exercise caused an increase in severity and/or extent of resting perfusion abnormalities in a greater proportion of patients of group 1 (53% vs 23%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Assessment of viability after myocardial infarction. Clinical relevance and methodological problems.

In patients with myocardial infarction, the distinction between reversible and irreversible ventricular dysfunction has important clinical implications since dysfunctional but viable myocardium will resume contraction following revascularization. Various methods have been developed for the identification of potentially reversible myocardial dysfunction. Thallium reinjection, immediately after stress-redistribution imaging, may provide evidence of myocardial viability by demonstrating thallium uptake in regions with apparently 'irreversible' defects. Hypoperfused, hypocontractile segments may recover function after revascularization, when exhibiting increased 18F-fluoro-deoxy-glucose uptake on positron emission tomography. Improved contractile function by selective beta 1 adrenergic stimulation with low dose dobutamine may also indicate the presence of viable tissue and predict subsequent improvement upon restoration of adequate flow. Finally, exercise-induced ST segment elevation on leads exploring a recent myocardial infarction has also been shown to indicate the presence of viable, potentially salvageable tissue. We discuss here these and several other methods that have been proposed for the detection of residual myocardial viability. Their advantages, limitations, and relevance to clinical problems are also discussed.

Cell Survival↗
PubMed1993

Metabolic management of ischaemic heart disease.

The present review summarizes the available information on the effects of the three major classes of antianginal agents (nitrates, calcium and beta-blockers) on myocardial energy metabolism. It also discusses the role of some new molecules (L-carnitine, trimetazidine and ranolazine) that have been proposed as an alternative pharmacological approach for the metabolic management of cardiac ischaemic syndromes.

Acetanilides↗
PubMed1993

[An aneurysm of the interatrial septum and cerebral embolic events: a clinical case and review of the literature].

Previous reports have described an association between atrial septal aneurysm and cerebral embolic events. We report the case of 68-year-old woman who was referred for evaluation of two syncopal episodes that had occurred within the previous three months. Physical examination, 12-lead ECG and exercise stress test were unremarkable; a 24-hour Holter monitoring did not show cardiac arrhythmias, and carotid ultrasonography excluded atherosclerotic lesions. Magnetic resonance imaging of the brain revealed multiple areas of decreased tissue density. Two-dimensional transthoracic echocardiography showed an atrial septal aneurysm that was confirmed by transesophageal imaging, which improved its morphologic characterization and ruled out the possibility of other atrial abnormalities with embolic potential. In conclusion, the syncopal episodes observed in our patient were likely due to cerebral embolism. This observation confirms the relation between atrial septal aneurysm and cerebrovascular ischemic events. As previously indicated, the presence of this abnormality dictates the need for anticoagulant therapy.

Aged↗
PubMed1992

Prevalence of silent myocardial ischaemia during exercise stress testing. Its relation to effort tolerance and myocardial perfusion abnormalities.

The number of underperfused myocardial segments, the extent of coronary artery disease and the severity of impairment of coronary flow reserve were compared in 147 consecutive patients exhibiting painful or painless ischaemic ST segment depression on exercise testing. Of 147 patients, only 61 (41%) experienced angina (group 1) whilst 86 (59%) did not (group 2). In the two groups coronary disease was comparable for both extent and distribution, and neither the location of transient perfusion defects nor their relation to areas of old myocardial necrosis appeared to influence the presence or absence of chest pain. However, exercise duration, exercise time and rate-pressure product at the beginning of ischaemia were lower in group 1. Furthermore, a greater proportion of asymptomatic patients had only one ischaemic segment on 99mTc-MIBI perfusion scintigraphy. We conclude that: (1) in patients with effort angina and coronary disease, the incidence of electrocardiographic silent ischaemic events induced by exercise is similar to that observed in studies based on continuous ECG monitoring. (2) Exertional angina is more frequently associated with greater ischaemic areas and with more severe degrees of impairment of residual coronary flow reserve. (3) The presence of an old myocardial infarction does not appear to influence the incidence of ischaemic cardiac pain.

Adult↗
PubMed1992

99Tcm-MIBI single photon emission tomography (SPET) for detecting myocardial ischaemia and necrosis in patients with significant coronary artery disease.

The ability of 99Tcm-methoxyisobutylisonitrile (MIBI) single photon emission tomography (SPET) to detect myocardial ischaemia and necrosis was assessed in 56 patients (45 male, 11 female, aged 55 +/- 5 years), with clinically recognized ischaemic heart disease (IHD). All underwent coronary angiography (CA) and left ventriculography (LV). SPET images were obtained at rest and at peak exercise (Modified Bruce) 90 min after injection of 99Tcm-MIBI (650-850 MBq). Data were acquired in 30 min over 180 degrees (from 45 degrees RAO to 45 degrees LPO) with no correction for attenuation, using a 64 x 64 matrix. The presence of persistent (P) or reversible (R) perfusion defects (PD) was then correlated to the resting and exercise ECG and to the results of CA and LV. Of the 56 patients, 34 had reversible underperfusion (RPD), 46 persistent underperfusion (PPD) and 31 had both. The occurrence of RPD correlated well with the occurrence of exercise-induced ST segment depression and/or angina (27 patients of 34 patients, 79%) and with the presence of significant coronary artery disease (CAD) (33 of 44, 73%). In 45 of 46 patients (98%) PPD corresponded to akinetic or severely hypokinetic segments (LV) usually explored by ECG leads exhibiting diagnostic Q waves (42 of 46 patients, 91%). The scan was normal both at rest and after stress in four of 11 patients with no CAD, and in two of 45 patients with CAD. Finally, an abnormal resting scan was seen in seven of 11 patients with normal coronary arteries, of whom six had regional wall motion abnormalities.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Symptom-limited exercise testing causes sustained diastolic dysfunction in patients with coronary disease and low effort tolerance.

Exercise stress testing is routinely used for the noninvasive assessment of coronary artery disease and is considered a safe procedure. However, the provocation of severe ischemia might potentially cause delayed recovery of myocardial function. To investigate the possibility that maximal exercise testing could induce prolonged impairment of left ventricular function, 15 patients with angiographically proved coronary disease and 9 age-matched control subjects with atypical chest pain and normal coronary arteries were studied. Radionuclide ventriculography was performed at rest, at peak exercise, during recovery and 2 and 7 days after exercise. Ejection fraction, peak filling and peak emptying rates and left ventricular wall motion were analyzed. All control subjects had a normal exercise test at maximal work loads and improved left ventricular function on exercise. Patients developed 1 mm ST depression at 217 +/- 161 s at a work load of 70 +/- 30 W and a rate-pressure product of 18,530 +/- 4,465 mm Hg x beats/min. Although exercise was discontinued when angina or equivalent symptoms occurred, in all patients diagnostic ST depression (greater than or equal to 1 mm) developed much earlier than symptoms. Predictably, at peak exercise patients showed a decrease in ejection fraction and peak emptying and filling rates. Ejection fraction and peak emptying rate normalized within the recovery period, whereas peak filling rate remained depressed throughout recovery (p less than 0.002) and was still reduced 2 days after exercise (p less than 0.02). In conclusion, in patients with severe impairement of coronary flow reserve, maximal exercise may cause sustained impairement of diastolic function.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Dissociation of platelet activation and spontaneous myocardial ischemia in unstable angina.

A dynamic thrombotic process, coronary spasm or both can be responsible for recurrent episodes of transient reduction of coronary blood flow in unstable angina. We have investigated the temporal relationship between episodic platelet activation, as detected by increased urinary excretion of 11-dehydro-TXB2, and spontaneous myocardial ischemia, assessed by continuous electrocardiographic monitoring and recording in 21 patients with unstable angina pectoris. In order to validate measurements of metabolite excretion as a reflection of intracoronary platelet activation, we have also performed repeated urine sampling from 8 patients undergoing PTCA and from 6 patients with peripheral vascular disease. The latter showed a 16% coefficient of variation in 3 consecutive 8-h urine samples. 11-dehydro-TXB2 increased significantly, by up to 15-fold, in the 2.5- to 5.0-h urine collection encompassing PTCA and decreased by greater than 50% during the following 2-h period. Patients with unstable angina were characterized by episodic increases (greater than 2 SD of controls) in metabolite excretion, in successive 6-8 h specimens. Paired measurements of 11-dehydro-TXB2 and 2,3-dinor-TXB2 in 15 urine samples did not reveal evidence of altered metabolic disposition of endogenously released TXB2. A total of 125 ECG ischemic episodes were recorded, of which 64% asymptomatic. We have compared these biochemical and ECG changes in patients randomized to i.v. low-dose aspirin or i.v. isosorbide dinitrate and oral diltiazem. Twenty-five of 56 (i.e. 45%) urine samples obtained in aspirin-free periods showed increased metabolite excretion as compared to 15 of 88 (i.e. 17%) samples collected during aspirin.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

Very early prediction of restenosis after successful coronary angioplasty: anatomic and functional assessment.

To investigate the time course of restenosis, serial treadmill exercise testing was performed in the absence of medical therapy by 31 patients with single vessel coronary disease who underwent successful angioplasty. Exercise tests were performed before angioplasty and at 3 days and 1, 3 and 6 months after angioplasty; if the test was positive, it was repeated after administration of 10 mg of intravenous verapamil. At arteriography 6 months after coronary angioplasty, 17 patients (group 1) showed no restenosis but 14 patients (group 2) did. Before angioplasty all 31 patients had a positive exercise test with ST segment depression greater than or equal to 1 mm. At 3 days after angioplasty, three patients in group 1 had a positive exercise test compared with 11 patients in group 2 (p = 0.08). At 1, 3 and 6 months, 1 patient in group 1 had a positive exercise test compared with 14 patients in group 2 (p less than 0.01). The heart rate-blood pressure product (beats/min.mm Hg) calculated at 1 mm ST segment depression, or at peak exercise if the test was negative, was used as an index of the ischemic threshold. In group 1 (no restenosis) the ischemic threshold increased progressively from 14,840 +/- 1,075 (mean value +/- SEM) before angioplasty to 21,210 +/- 1,049 at 3 days and to 25,140 +/- 1,177 (p less than 0.001) at 6 months. In group 2 (restenosis) the ischemic threshold increased from 16,270 +/- 828 before angioplasty to 20,400 +/- 984 (p less than 0.0004) at 3 days but decreased to 16,090 +/- 1,298 (p less than 0.006) at 6 months.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Combined effects of nitrates on the coronary and peripheral circulation in exercise-induced ischemia.

We compared the effects of isosorbide dinitrate (ISDN) administered by intracoronary and intravenous routes in 10 patients with severe coronary artery disease, stable effort angina, and very low exercise tolerance. Supine bicycle ergometer exercise was performed under four conditions: 1) control, 2) after intracoronary administration of 0.4 mg ISDN, 3) 1 hour later (control 2), and 4) after administration of intravenous 4 mg ISDN. At rest, intracoronary ISDN caused no significant hemodynamic effects, whereas intravenous infusion of ISDN resulted in a decline in left ventricular (LV) systolic pressure (-20 +/- 5 mm Hg), LV end-diastolic volume (-27 +/- 3%), and LV end-systolic volume (-30 +/- 4%). After intracoronary infusion of ISDN, ST segment depression and the increase in LV end-diastolic pressure and LV end-systolic volume induced by exercise were significantly less abnormal than during control (0.20 +/- 0.09 vs. 0.14 +/- 0.08 mV, 36 +/- 7 vs. 24 +/- 8 mm Hg, and 91 +/- 40% vs. 40 +/- 29%, respectively). When exercise was performed after intravenous infusion of ISDN, the above-mentioned parameters were significantly improved even further: ST segment depression to 0.05 +/- 0.07 mV, end-diastolic pressure to 14 +/- 7 mm Hg, and LV end-systolic volume to 5 +/- 11% (all p less than 0.01 compared with intracoronary ISDN). Thus, in patients with severe coronary artery disease, it is suggested that intracoronary nitrates increase coronary blood supply during effort-induced ischemia, based on significant improvements in the indirect measures of ST segment depression, LV end-diastolic pressure, and LV volume.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗
PubMed1988

Sequence and magnitude of ventricular volume changes in painful and painless myocardial ischemia.

Stimulation of left ventricular stretch receptors has been proposed as a possible mechanism for the occurrence of cardiac pain. Changes in left ventricular volume were continuously assessed in 12 patients during 11 spontaneous (two painful) and 12 ergometrine-induced (nine painful) ischemic attacks with a precordial scintillation probe and blood pool labeling with technetium-99m. In all ischemic episodes, spontaneous or induced, painful or painless, severe dilatation of the left ventricle was consistently observed. These changes always preceded the onset of ST segment shifts and occurred long before pain, when present. The maximum increase in end-diastolic volume was slightly greater in painful than in painless episodes, 38 +/- 8.0% versus 28 +/- 12.4%, but no significant difference was observed in the rate of volume change or in the maximum increase of end-systolic volume (133 +/- 50% and 110 +/- 27.3%), stroke volume (-28 +/- 15% and -25 +/- 12.4%), or ejection fraction (-32 +/- 8.7% and -26 +/- 6.0%). Although the maximum end-diastolic volume achieved is greater in painful episodes, this effect cannot be separated from that of duration, and, furthermore, there was no significant difference in end-diastolic volume at the moment chest pain began. Thus, in patients with angina at rest, transient asymptomatic ST segment shifts are consistently associated with large changes in left ventricular volume, similar to those observed during painful episodes. The rate and extent of acute left ventricular dilatation do not appear to be factors directly causing anginal pain.

Angina Pectoris↗
PubMed1988

Prevalence of parathyroid insufficiency after thyroidectomy: study of 1037 cases.

In 1037 patients undergoing total (827 cases) or partial thyroidectomy (52 cases of subtotal thyroidectomy, 108 of hemithyroidectomy, 50 of enucleation and resection) for each study group the incidence of hypoparathyroidism, its possible causes and technical factors favouring the onset, were examined. In this series postoperative prevalence of hypoparathyroidism was 16.6%. It seems to be directly proportional to the extent of surgery thus confirming the necessity to locate and preserve the parathyroid glands during surgery. This should be as conservative as possible according to the prognosis of the thyroid disease.

Cross-Sectional Studies↗
PubMed1987

Relative roles of preload increase and coronary constriction in ergonovine-induced myocardial ischemia in stable angina pectoris.

To assess the relative role of increased ventricular preload and critical coronary lesions in ergonovine-induced myocardial ischemia, 9 normal subjects (group A), 7 patients with stable angina (group B) and 5 with variant angina (group C) were studied. In all patients, the 12-lead electrocardiogram, blood pressure and left ventricular (LV) volume (technetium-99m blood pool) were continuously recorded before and during administration of incremental doses of ergonovine given at 5-minute intervals. In all subjects, an initial LV dilatation developed; in group B and C patients, this was followed by a decrease in stroke volume and ejection fraction with subsequent onset of electrocardiographic changes and angina. The interval between these events was significantly shorter in group C and in 3 group B patients; in these patients, signs of ischemia appeared with smaller ergonovine doses and at minimal preload increase, coronary constriction being the likely mechanism of ischemia. In the remaining 4 group B patients, the onset of stroke volume, ejection fraction, electrocardiographic changes and angina was significantly delayed, occurring after administration of larger ergonovine doses when LV volume was already considerably increased. This finding suggests that the loading effect of ergonovine on LV volume, rather than on coronary constriction, could be the prevailing mechanism of ergonovine-induced ischemia in these patients.

Angina Pectoris↗
PubMed1987

Usefulness of Holter monitoring to improve the sensitivity of exercise testing in determining the degree of myocardial revascularization after coronary artery bypass grafting for stable angina pectoris.

To assess whether Holter monitoring improves the sensitivity of exercise testing in identifying incomplete myocardial revascularization, both tests were performed in 45 patients from 3 to 5 months after elective coronary artery bypass grafting (CABG) for stable angina pectoris. Coronary angiography revealed incomplete revascularization in 26 patients. Six of these 26 had 52 episodes of ST-segment depression during Holter monitoring and myocardial ischemia during exercise testing. Their exercise capacity was significantly lower than that of 10 other patients in whom the results of exercise testing only were positive (heart rate at 0.1 mV ST-segment depression 112 +/- 9 vs 123 +/- 15 beats/min, p less than 0.001). In the other 10 patients with incomplete myocardial revascularization the results of both investigations were negative. The graft patency rate was lower in patients with a positive response to exercise testing than in those with a negative response (52% vs 71%, p less than 0.005). Myocardial revascularization was angiographically complete in 19 patients. In 18 of these 19 patients the findings of both investigations were negative; in 1 patient Holter monitoring revealed episodes of ST-segment elevation suggestive of variant angina. Thus, after CABG for stable angina pectoris the results of Holter monitoring do not improve the sensitivity of exercise testing in identifying patients with angiographically incomplete myocardial revascularization because findings are positive only in patients with low exercise capacity. Both tests fail to show evidence of myocardial ischemia in most patients with angiographically complete myocardial revascularization.

Aged↗