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E Poma

Publications and source records attributed to E Poma.

14 recordsLinked to original sources
PubMed1993

Human cytomegalovirus immediate-early gene 2 protein interacts with itself and with several novel cellular proteins.

The human cytomegalovirus immediate-early gene product 2 (IE2) is able to transactivate homologous and heterologous promoters alone or augmented by immediate-early gene product 1 (IE1). IE2 has also been shown to autoregulate the major immediate-early promoter by directly binding to a cis repression signal located between the TATA box and the cap site. However, IE2 has not been shown to act directly through a specific DNA sequence in transactivating various promoters. To understand whether IE2 can be indirectly involved in DNA sequence-specific transactivation through interactions with other transcriptional factors, we performed a study of the interactions of IE2 with cellular proteins. In order to study these interactions, IE cDNAs were subcloned into a bacterial expression vector, pGEX2T, by polymerase chain reaction amplification to produce fusion proteins which were full-length as well as proteins which contained various functional domains. We were able to demonstrate IE2's ability to interact directly or indirectly with several cellular proteins ranging from > 200 to 14 kDa through glutathione S-transferase-fusion protein precipitation and far-Western analysis. These interactions have been mapped to domains within IE2 which are known to be necessary for either transactivation or both transactivation and autoregulation. All of the IE2-associated proteins are nuclear proteins, and a subset are phosphorylated. In vitro-synthesized 35S-IE2 protein and bacterially expressed IE2 fusion proteins were used to study IE2-IE2 interaction by binding assay and far-Western analysis. IE2-IE2 interactions were mapped to a domain containing a putative helix-turn-helix motif located near the C terminus of IE2, between amino acids 456 and 539. However, IE2 was unable to directly interact with either IE1, an alternatively spliced variant of IE2 (55 kDa), or IE2 deletion mutants that did not contain the multimerization domain.

Amino Acid Sequence↗
PubMed1989

Long-term survival and risk stratification in patients with angina at rest undergoing medical treatment.

In order to determine those factors which influence long-term prognosis in patients with angina at rest associated with transient ST-segment changes, 217 patients undergoing medical treatment were followed for a mean of 39 months. All patients underwent coronary arteriography. Univariate analysis identified 12 variables significantly related to prognosis. These were disease of the left main coronary artery; the number of diseased vessels; left ventricular end-diastolic pressure; ejection fraction; baseline electrocardiogram; presence of prior myocardial infarction; ST-segment depression and ventricular arrhythmias during pain; disease of the proximal anterior descending coronary artery; crescendo angina; hypertension; and age. Use of the Cox regression model for survival analysis revealed only 3 variables which were independent predictors of prognosis. They were disease of the left main coronary artery; the number of diseased vessels and left ventricular end-diastolic pressure. The model allowed stratification of patients into 3 groups. Survival at 3 years was 98% in the low risk group; 82% in the intermediate risk group; and 58% in the high risk group. These data indicate that disease of the left main coronary artery, the number of diseased vessels and left ventricular end-diastolic pressure are the independent predictors of prognosis in angina at rest. These variables may allow stratification of patients into groups having different long-term survivals.

Adult↗
PubMed1988

Acute haemodynamic effects of diltiazem in patients with recent Q-wave myocardial infarction.

The effects of diltiazem on left ventricular systolic and diastolic function were studied in 14 patients with a recent (12-20 days) Q-wave myocardial infarction. Left ventriculography with simultaneous recording of high-fidelity left ventricular pressure was performed in control conditions, and after i.v. administration of diltiazem (0.2 mg kg-1 as a bolus followed by constant infusion of 0.005 mg kg-1 min-1 lasting 8-10 min). After the administration of the drug, left ventricular systolic pressure decreased by 12.7% and mean circumferential wall stress by 14% (both P less than 0.01); the heart rate did not change; the ejection fraction increased by 9.6% (P less than 0.05) and maximum dP/dt/P by 11% (P less than 0.01). Quantitative segmental wall motion analysis showed that the beneficial effects of diltiazem on global left ventricular systolic function were associated with an increase in contraction in hypokinetic regions, where they were supplied by normal or diseased coronary vessels (both P less than 0.01). Left ventricular end-diastolic pressure decreased by 23.6% (P less than 0.05) and minimal diastolic pressure by 38% (P less than 0.05). Passive diastolic properties of the left ventricular chamber remained unaltered but isovolumic relaxation markedly improved: the T constant decreased 26% (P less than 0.01). Thus, in patients with a recent Q-wave myocardial infarction, the i.v. administration of diltiazem unloads the left ventricular chamber without showing depressant effects on myocardial contractility.

Adult↗
PubMed1988

Clinical significance of mitral regurgitation in patients with recent myocardial infarction.

The prognostic implications of the presence of mitral regurgitation (MR) in patients with recent myocardial infarction has not been clarified yet. In March 1983, we undertook a prospective study in patients surviving a first episode of acute myocardial infarction. Over a 4-year period, 266 patients entered the study. Left ventriculography documented the presence of MR in 51 patients, while 215 did not have angiographic evidence of MR. The presence of MR was associated with larger infarcts, as shown by greater values of peak CK (P less than 0.05) and by the prevalence of Q-wave vs non-Q-wave infarctions (P less than 0.05). Transient left ventricular failure during hospitalization was more frequent in patients with MR (P less than 0.05), while the occurrence of early post-infarction angina was similar in the two groups of patients. No difference was found in the extent of coronary disease, yet patients with MR had higher values of left ventricular end diastolic pressure (LVEDP) (P less than 0.005) and a lower ejection fraction (EF) (P less than 0.001). Patients with MR had a reduced exercise capacity (P less than 0.005), but signs of myocardial ischaemia were similarly distributed in the two groups. Patients with anterior infarcts and MR had higher left ventricular volumes than patients without MR, while no difference was found between patients with and patients without MR and inferior infarction, suggesting that left ventricular dilatation may play an important role in the pathogenesis of MR in patients with anterior but not in those with inferior infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Angiography↗
PubMed1988

Effects of surgical versus medical treatment on long-term prognosis in angina at rest: an observational non-randomized study of 400 patients.

The effect of surgical versus medical treatment on long-term prognosis in angina at rest was assessed using the Cox regression model for survival analysis in 400 patients complaining of recurrent episodes of resting chest pain associated with transient repolarization changes. The surgical group included 185 patients, and the medical group 215. Surgically treated patients more frequently had two- and three-vessel disease, while single-vessel disease prevailed in medically treated patients (P less than 0.01). No difference between the two groups was found in mean values of left ventricular end diastolic pressure and ejection fraction. Three variables were identified as independent predictors of prognosis in all patients: left ventricular end-diastolic pressure (P less than 0.001), age greater than 45 years (P less than 0.05), and number of diseased vessels (P less than 0.05). Treatment modality did not result in different long-term survival in the entire population. However, patients with three-vessel disease had a better outcome with surgical than with medical therapy (P less than 0.05). Although our conclusions must be tempered by consideration of the limitations of non-randomized studies, these results show that surgical treatment may improve survival in patients with angina at rest and three-vessel disease.

Angina Pectoris↗
PubMed1988

Unstable angina.

Patients with unstable angina, defined as resting chest pain associated with transient repolarization changes on the electrocardiogram, represent a high risk subset among the clinical manifestations of ischemic heart disease. Pathogenetic mechanisms include coronary spasm and vasoconstriction, coronary thrombosis and platelet aggregation. Early prognosis is related to the degree of activity of the disease while long-term outcome depends on the extent of the coronary disease and the degree of left ventricular dysfunction. Medical treatment should include the combination of beta-blockers, nitrates and calcium antagonists as well as the use of heparin and aspirin. Despite such an aggressive treatment, attacks of resting chest pain persist in almost 30 per cent of patients. In these cases emergency revascularization may be achieved by either coronary angioplasty or bypass surgery. The latter operation may result in improved survival in patients with impaired left ventricular function and triple vessel disease.

Angina Pectoris↗
PubMed1988

[Relationship between morphology of restenosis and clinical aspects in patients who had undergone coronary angioplasty].

Although restenosis after percutaneous transluminal coronary angioplasty (PTCA) may have morphologic characteristics which are not similar to the original stenosis, it is unknown if a different morphology is also associated with a different clinical presentation. Eleven consecutive patients with angina and single vessel disease had a recurrence of symptoms and restenosis within 6 months of successful PTCA. Seven patients (group I) complained of spontaneous angina before PTCA and had a positive hyperventilation test, while 4 patients complained of exercise-induced angina and had a negative hyperventilation test (group II). In group I restenosis was associated with the same clinical presentation as before PTCA and the hyperventilation test was positive in 6 patients. The angiographic morphology of restenosis was changed in 4 patients. In group II restenosis occurred with the same clinical presentation as before PTCA, the hyperventilation test was negative in 3 patients while the angiographic morphology of restenosis was unchanged in only 1 patient. Although morphology of restenosis is different from the original stenosis, clinical presentation associated with restenosis is generally the same as before PTCA. The response to vasoactive stimuli is independent from the morphology of the lesion.

Angina Pectoris↗
PubMed1987

Coronary vasoconstrictor response to cold pressor test in variant angina: lack of relation to intracoronary thromboxane concentrations.

To test the hypothesis that intracoronary concentrations of thromboxane (Tx)A2 could influence the response to cold pressor test (CPT) in variant angina, great cardiac vein blood flow (by thermodilution) and the concentration of TxB2 (the stable metabolite of TxA2) in the great cardiac vein and aorta were measured under control conditions and during CPT in 14 patients with angina at rest associated with transient ST-segment elevation in the anterior leads. In seven patients pretreated with aspirin (intravenous administration of 3.6 mg/kg lysine salt of acetylsalicylic acid, corresponding to 2 mg/kg aspirin), TxB2 baseline concentrations were lower in both the great cardiac vein (47 +/- 19 vs 176 +/- 88 pg/ml; p less than 0.005) and the aorta (45 +/- 16 vs 109 +/- 56 pg/ml, p less than 0.02) than in seven patients who were not taking cyclooxygenase inhibitors. In the two groups, great cardiac vein flow and anterior region coronary resistance were similar under control conditions. During CPT anterior region coronary resistance increased in patients pretreated with aspirin (from 1.97 +/- 0.99 to 2.22 +/- 1.11 mm Hg/ml/min; p less than 0.02) and in patients without aspirin pretreatment (from 1.94 +/- 0.43 to 2.06 +/- 0.34 mm Hg/ml/min; p less than 0.05), and the difference between the two groups was not statistically significant. Therefore the vasoconstrictor response of coronary vessels to CPT in variant angina is not influenced by the intracoronary TxB2 concentrations and is not modified by aspirin pretreatment.

Adult↗
PubMed1987

Clinical significance of exercise-induced silent myocardial ischemia in patients with coronary artery disease.

Exercise-induced silent myocardial ischemia is a frequent feature in patients with coronary artery disease. The purpose of this study was to compare the clinical and angiographic characteristics of 269 patients who complained of chest pain during an exercise test (group I) with those of 204 who developed exercise-induced silent myocardial ischemia (group II). Group I patients more frequently had anginal symptoms of class III and IV of the Canadian Cardiovascular Society than did group II patients, who had milder symptoms (p less than 0.001). The only angiographic difference observed between the two groups was a slightly but significantly higher left ventricular end-diastolic pressure in group II patients (p less than 0.05), who also showed a longer exercise duration (p less than 0.01) with a higher heart rate-systolic pressure product (p less than 0.01) and more pronounced ST segment depression at peak exercise (p less than 0.001). Moreover, ventricular ectopic beats during exercise were more frequently observed in group II patients (p less than 0.05). Coronary bypass surgery was performed in 45% of patients of group I and in 24% of patients of group II (p less than 0.05). Survival curves of medically treated patients did not show any statistically significant difference between the two groups. Thus, although patients with a defective anginal warning system may have more pronounced signs of myocardial ischemia and a greater incidence of ventricular arrhythmias during exercise, their long-term prognosis is not different from that of patients who are stopped by angina from the activity that is inducing myocardial ischemia.

Coronary Angiography↗
PubMed1987

Coronary haemodynamic effects of short-term intravenous administration of gallopamil in patients with stable exertional angina.

The effects of short term intravenous administration of gallopamil on coronary haemodynamic variables were studied in 10 patients with stable exertional angina and angiographically confirmed coronary artery disease that affected the proximal portion of the left anterior descending artery. Blood flow in the great cardiac vein was measured by a thermodilution technique, both at rest and during ischaemia induced by atrial pacing, before and after intravenous administration of gallopamil (0.02 mg/kg as a bolus dose given over three minutes, followed by an infusion of 0.0005 mg/kg/min). Gallopamil significantly prolonged the mean (SD) duration of pacing that was tolerated (11 (2.6) vs 14.8 (2.4] min, significantly increased the mean (SD) peak heart rate attained during pacing (142 (15) vs 158 (11) beats/min), and reduced mean (SD) arterial pressure (133 (17) vs 116 (17) mm Hg). There were no changes in mean (SD) blood flow in the great cardiac vein (134.1 (57) vs 112.9 (38) ml/min, mean (SD) anterior regional coronary resistance (1.18 (0.6) vs 1.15 (0.5) mm Hg/ml/min), and mean (SD) anterior regional myocardial oxygen consumption (16.6 (6) vs 13.7 (4) ml/min). These data confirm that gallopamil is an effective antianginal agent and suggest that a reduction of myocardial oxygen demand is the predominant mechanism by which the drug exerts its beneficial effects.

Angina Pectoris↗
PubMed1986

Clinical and angiographic data in early post-infarction angina.

The preliminary results of a prospective study undertaken in patients with a first episode of acute myocardial infarction are presented. The clinical, electrocardiographic and angiographic characteristics of 34 patients who developed early post-infarction angina (group I) were compared with those of 144 patients who remained asymptomatic after the acute infarct (group II). No difference was found between the two groups as to age, sex prevalence, risk factors, presence of stable angina before infarction, severe ventricular arrhythmias or transient congestive heart failure in CCU and peak CK value. Patients of group I had more frequently ecg signs of myocardial infarction in anterior leads (P less than 0.01) than patients of group II. Exercise testing, performed by 23 patients of group I and by 140 patients of group II, was positive in 14 patients with early post-infarction angina and in 37 who remained asymptomatic after the acute infarct (P less than 0.01). The two groups had similar values of left ventricular end diastolic volume index, left ventricular end diastolic pressure and ejection fraction. Patients with early post-infarction angina however had more frequently double or triple vessel disease, while single vessel disease prevailed in group II patients. Although the follow-up period was limited (average 9 months), a higher incidence of cardiac complications was found in group I patients (P less than 0.01). These data show that early post-infarction angina defines a high-risk subset of patients among those with recent myocardial infarction. A more aggressive approach, including thrombolytic therapy and coronary angioplasty, seems warranted.

Angina Pectoris↗
PubMed1986

Effects of diltiazem on regional coronary hemodynamics during atrial pacing in patients with stable exertional angina: implications for mechanism of action.

To investigate the mechanism of the antianginal action of diltiazem in stress-induced myocardial ischemia, we studied 12 patients with stable exertional angina and disease of the proximal left anterior descending artery by measuring great cardiac vein flow (GVCF) and calculating anterior regional coronary resistance (ARCR) during myocardial ischemia induced by atrial pacing before and after intravenous administration of diltiazem (0.25 mg/kg in a bolus dose followed by continuous infusion of 0.005 mg/kg/min). Diltiazem increased the pacing time to angina from 6.9 +/- 3.5 to 10.7 +/- 4 min (p less than .001). At peak pacing heart rate was increased after diltiazem (from 128 +/- 17 to 145 +/- 17 beats/min, p less than .005), while mean arterial pressure was decreased (from 131 +/- 19 to 113 +/- 17 mm Hg, p less than .025), leaving the double product unaltered. At peak pacing no changes were observed in GCVF (from 115 +/- 46 to 119 +/- 46 ml/min, p = NS), ARCR (from 1.3 +/- 0.4 to 1.1 +/- 0.4 mm Hg/ml/min), or myocardial oxygen consumption of the anterior region (from 14.5 +/- 4.2 to 13.4 +/- 4.7 ml/min). Reduction of myocardial oxygen demand plays a major role in the antianginal action of diltiazem in patients with stress-induced myocardial ischemia.

Adult↗
PubMed1986

Clinical application of monitoring techniques: coronary sinus blood flow monitoring.

Measurement of coronary sinus blood flow by continuous thermodilution is a well established technique for the clinical study of myocardial perfusion. More recently, advances in catheter technology enabled regional left ventricular flow measurements. In particular, measurement of flow from the great cardiac vein appears to accurately reflect the perfusion of the left anterior descending coronary artery. This regional approach allowing the correlation with coronary arterial anatomy, has contributed to an improved understanding of the mechanisms by which functional factors interact with organic narrowing in the genesis of myocardial ischemia at rest, during provocative tests and during exercise. In addition, it has provided useful information in the evaluation of antianginal drugs through the discrimination between the effects on coronary resistance and myocardial oxygen consumption.

Angina Pectoris↗