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Biomedical subjects

A G Rebuzzi

Publications and source records attributed to A G Rebuzzi.

At least 37 records · Page 2Linked to original sources
PubMed1996

Temporal relation between ischemic episodes and activation of the coagulation system in unstable angina.

BACKGROUND: Although a major role of coronary thrombosis in the pathogenesis of unstable angina has been demonstrated, the results of a series of studies have suggested that activation of the hemostatic system may not be confined to ischemic episodes. The purpose of this study was to investigate the temporal relation between ischemic episodes and activation of the coagulation system in unstable angina. METHODS AND RESULTS: Thrombin-antithrombin III (TAT) and prothrombin fragment 1 + 2 (F1 + 2) levels were measured in 13 patients during spontaneous ischemic episodes (time 0, 5, and 15 minutes and 1 hour) to evaluate the time course of the activation of the coagulation system associated with the development of ischemia (protocol A). TAT and F1 + 2 levels were also measured in 28 patients with unstable angina on admission to hospital (every 6 hours for 24 hours and daily for 3 days) to assess their temporal relation with ischemic episodes (protocol B). In protocol A, TAT and F1 + 2 levels were elevated in 10 of 13 patients (77%) in at least 1 sample. The median value of TAT showed a peak at 5 minutes and returned to baseline within 15 minutes (P < .05), consistent with its plasma half-life of 5 minutes, whereas the median value of F1 + 2 showed no significant changes, possibly because of its longer half-life, which tends to dampen sudden bursts of thrombin production. In protocol B, activation of the clotting system was found in 10 of 33 samples (30%) temporally related to ischemia and also in 23 of 150 (15%, P = .07) of those not temporally related to ischemia. CONCLUSIONS: Our study demonstrates that patients with active unstable angina develop frequent bursts of thrombin production not necessarily associated with ischemic episodes and that, conversely, some ischemic episodes are not associated with evidence of thrombin activation.

Adult↗
PubMed1996

Intracellular neutrophil myeloperoxidase is reduced in unstable angina and acute myocardial infarction, but its reduction is not related to ischemia.

OBJECTIVES: This study sought to assess neutrophil activation in acute coronary syndromes and its relation to ischemic episodes. BACKGROUND: Neutrophil activation has been reported in unstable angina and acute myocardial infarction; however, it is not clear whether it is related exclusively to ischemia-reperfusion injury. METHODS: We measured the index of intracellular myeloperoxidase in 1) patients with unstable angina, myocardial infarction, variant angina and chronic stable angina and in normal subjects (protocol A); and 2) in patients with unstable angina and acute myocardial infarction during the first 4 days of the hospital period (protocol B). To assess whether neutrophil activation was triggered by ischemia, the myeloperoxidase intracellular index was analyzed before and after spontaneous ischemic episodes and before and after ischemia induced by an exercise stress test in 10 patients with chronic stable angina. In 11 patients with unstable angina, we also compared values of the myeloperoxidase intracellular index at entry with those after waning of symptoms. RESULTS: In protocol A, the myeloperoxidase intracellular index was significantly reduced in patients with unstable angina and acute myocardial infarction compared with patients with stable and variant angina and normal subjects (p < 0.01). In protocol B, the myeloperoxidase intracellular index did not change over time in patients with unstable angina and myocardial infarction. However, in 11 patients with waning symptoms, the myeloperoxidase intracellular index was significantly higher afer symptoms had waned (p < 0.05). In patients with unstable angina, 23 ischemic episodes were studied; no changes in the myeloperoxidase intracellular index were observed. In 10 patients with chronic stable angina and positive exercise stress test results, no significant differences in the myeloperoxidase intracellular index were observed after stress-induced ischemia. CONCLUSIONS: Our study confirms that neutrophils are activated in acute coronary syndromes but suggests that their activation may not be only secondary to ischemia-reperfusion injury.

Adult↗
PubMed1994

The prognostic value of C-reactive protein and serum amyloid a protein in severe unstable angina.

BACKGROUND: The pathogenesis of unstable angina is poorly understood, and predicting the prognosis at the time of hospital admission is problematic. Recent evidence suggests that there may be active inflammation, possibly in the coronary arteries, in this syndrome. We therefore studied the prognostic value of measurements of the circulating acute-phase reactants C-reactive protein and serum amyloid A protein, which are sensitive indicators of inflammation. METHODS: We measured C-reactive protein, serum amyloid A protein, creatine kinase, and cardiac troponin T in 32 patients with chronic stable angina, 31 patients with severe unstable angina, and 29 patients with acute myocardial infarction. RESULTS: At the time of hospital admission, creatine kinase and cardiac troponin T levels were normal in all the patients, but the levels of C-reactive protein and serum amyloid A protein were > or = 0.3 mg per deciliter (exceeding the 90th percentile of the normal distribution) in 4 of the patients with stable angina (13 percent), 20 of the patients with unstable angina (65 percent), and 22 of the patients with acute myocardial infarction (76 percent). The 20 patients with unstable angina who had levels of C-reactive protein and serum amyloid A protein > or = 0.3 mg per deciliter had more ischemic episodes in the hospital than those with levels < 0.3 mg per deciliter (mean [+/- SD] number of episodes per patient, 4.8 +/- 2.5 vs. 1.8 +/- 2.4; P = 0.004); 5 patients subsequently had a myocardial infarction, 2 died, and 12 required immediate coronary revascularization. In contrast, no deaths or myocardial infarction occurred among the 11 patients with levels of C-reactive protein and serum amyloid A protein < 0.3 mg per deciliter, and only 2 of them required coronary revascularization. Among the patients admitted with a diagnosis of acute myocardial infarction, unstable angina preceded infarction in 14 of the 22 patients (64 percent) with levels of C-reactive protein and serum amyloid A protein > or = 0.3 mg per deciliter but in none of the 7 patients with levels < 0.3 mg per deciliter. CONCLUSIONS: Elevation of the sensitive acute-phase proteins C-reactive protein and serum amyloid A protein at the time of hospital admission predicts a poor outcome in patients with unstable angina and may reflect an important inflammatory component in the pathogenesis of this condition.

Angina Pectoris↗
PubMed1994

[Antithrombin therapy in acute coronary syndromes].

Intracoronary thrombosis is fundamental in the pathogenesis of acute coronary syndromes, although the causes of thrombosis are still unclear. As thrombin generation is crucial for thrombus formation, the inhibition of thrombin is a primary aim to prevent the evolution of an initial repair process into a pathological thrombus. Thrombin inhibition can be achieved by several drugs. Heparin is the principal antithrombin drug currently used in acute syndromes; it acts mainly by binding to antithrombin III and increasing its inhibitory effect on thrombin and other coagulation factors. The heparin-antithrombin III complex, however, does not inhibit thrombus-bound thrombin; moreover, iv heparin requires frequent laboratory monitoring and dose adjustments. Despite these limitations, continuous infusion of i.v. heparin has been found to be effective in unstable angina and in myocardial infarction, especially when treated with accelerated rt-PA. New antithrombin drugs that selectively and directly inhibit thrombin are hirudin, its synthetic derivate hirulog, and argatroban. These drugs have several theoretical advantages over heparin: greater stability of the aPTT--with the need for less laboratory monitoring--and greater efficacy--associated mainly with its capacity to inhibit clot-bound thrombin. Clinical pilot studies seem to indicate a greater antithrombotic efficacy compared with heparin, but a greater number of hemorrhagic events in patients with acute myocardial infarction receiving thrombolysis. In conclusion, the use of heparin is certainly indicated in patients with unstable angina and persistent ischemia and in acute myocardial infarction treated with accelerated rt-PA. The use of new antithrombin drugs, although promising, requires further clinical evaluation.

Acute Disease↗
PubMed1992

Importance of reperfusion on thromboxane A2 metabolite excretion after thrombolysis.

Fibrinolytic therapy is a major advance in the treatment of coronary artery disease. A marked elevation in plasma and urinary metabolites of thromboxane A2 (TXA2) after administration of thrombolytic therapy has been observed and has been related to a direct effect of thrombolytic drugs on platelets. To test this hypothesis we evaluated the 11-dehydro-thromboxane B2 (11-d-TXB2) level, as an index of platelet activation, in 20 healthy subjects and in 30 patients with acute myocardial infarction (AMI). Patients with infarction received streptokinase (n = 8), recombinant tissue-type plasminogen activator (rt-PA) (n = 8), or thrombolytic therapy preceded by acetylsalicylic acid (n = 7) or were treated without thrombolytic therapy (n = 7). The urinary 11-d-TXB2 level in healthy control subjects was 327 +/- 126 pg/mg creatinine. A significant increase was observed in patients with AMI with no difference between those who received no thrombolytic therapy (673 +/- 283 pg/mg creatinine in the first 12 hours) and those who received streptokinase (833 +/- 613 pg/mg creatinine) or rt-PA (836 +/- 653 pg/mg creatinine). Patients pretreated with acetylsalicylic acid had urinary 11-d-TXB2 values ranging between 361 and 155 pg/mg creatinine. A significant difference in 11-d-TXB2 values was observed only when patients who were reperfused were separated from those who remained occluded according to angiographic criteria (1085 +/- 498 vs 391 +/- 227 pg/mg creatinine in the first 12 hours, p less than 0.001). We conclude that reperfusion and not thrombolytic agents per se appears to be the factor that induces platelet activation and consequently facilitates reocclusion.

Aspirin↗
PubMed1990

Reproducibility in circadian rhythm of ventricular premature complexes.

To evaluate the existence and reproducibility of a circadian rhythm of ventricular premature complexes (VPCs), 38 patients (mean age 57 +/- 17 years) with greater than or equal to VPCs/hour were studied with 24-hour electrocardiogram Holter monitoring. Nineteen patients had coronary artery disease and 19 had structurally normal hearts. A second Holter electrocardiogram was recorded in all patients from 2 to 47 days (mean 11) after the first. Chronobiologic analysis was made by single and mean cosinor methods. A significant and similar circadian rhythm of VPCs was found in the total sample both on the first (mesor 399, acrophase at 15:08, p less than 0.01) and the second day (mesor 306, acrophase at 14:47, p less than 0.05), with 2 main peaks, the first in the late morning and the second in the afternoon. However, only 18 patients (47%, group A) had a significant individual circadian rhythm of VPCs on both days, whereas 20 (53%, group B) did not have a significant rhythm in greater than or equal to 1 day. A high reproducibility of the circadian rhythm of VPCs was found in group A patients, with a difference of 2.1 +/- 1.8 hours between the acrophases of the 2 days, whereas the difference was 4.4 +/- 3.3 hours in group B patients (p less than 0.01). Among group A patients, 14 (78%) had a VPC rhythm with acrophase occurring during waking hours, whereas the acrophase of 4 (22%) occurred during the night. The reproducibility of the circadian rhythm of VPCs was not influenced by gender, presence of coronary disease, medical therapy, basal VPC number, or day-to-day variability of VPCs, although group A patients were older than group B patients (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Accuracy in clinical arrhythmia detection of a real-time Holter system (Oxford Medilog 4500).

The accuracy of a real-time analysis Holter system (Oxford Medilog 4500) in detecting ventricular and supraventricular arrhythmias was evaluated. Hand-counted data from randomly selected hours of 152 ECG monitorings of 152 patients were used as the control standard. Accuracy of the system was evaluated on 606 hours for premature ventricular complexes (PVC), PVC couplets and supraventricular extrasystoles (SVE), and on 1,789 hours for ventricular tachycardia (VT), accelerated idioventricular rhythm (AIVR), and supraventricular tachycardia (SVT). Sensitivity and positive predictive accuracy for the Oxford system were (1) 92.9% and 94.9% for PVC; (2) 90.1% and 87.8% for PVC couplets; (3) 98.1% and 56% for AIVR; (4) 80% and 82.3% for VT; (5) 88.6% and 56.5% for SVE, and (6) 43.7% and 60.2% for SVT. Furthermore, negative predictive accuracy, the ability to predict the total absence of an arrhythmic event in an hour, was determined. It was 91.7% for PVC, 99.5% for PVC couplets, 99.9% for AIVR, 99.7% for VT, 95% for SVE, and 98% for SVT. ventricular arrhythmias, whereas significant inaccuracies appear to exist in the analysis of supraventricular arrhythmias.

Algorithms↗
PubMed1990

[rTPA and streptokinase in acute myocardial infarct. Clinical instrumental evaluation of the 2 treatments].

Fifty-four patients with acute myocardial infarction were treated with thrombolytic therapy (27 with rTPA and 27 with streptokinase). In all the subjects CK was monitored (every 3 hours) and ergometric test, echocardiogram, and 24 hours holter ecg were performed in the pre-discharge period. In 22 of the patients, coronary angiography was also performed. No differences were shown between the two groups of patients as regards CK values and ejection fraction. Repetitive ventricular premature beats were registered without difference between the two groups (23% in patients treated with SK and 18% in the patients treated with rTPA). No bleeding events were shown in the patients treated with rTPA without calciparin. On the other hand no difference there was between patients treated with rTPA + calciparin and patients treated with SK with or without calciparin.

Aged↗
PubMed1989

[Characteristics of non-sustained ventricular tachycardia found during dynamic ECG in patients with recent myocardial infarction].

The characteristics of ventricular tachycardia found during Holter ECG monitoring before discharge in patients hospitalized because of acute myocardial infarction were analyzed. One or more ventricular tachycardia episodes were found in 29 of 251 patients (11.5%). On the whole, there were 233 episodes of ventricular tachycardia: 18 patients (62%) had only one episode of ventricular tachycardia, 9 (31%) 2-5 episodes and 2, respectively, 68 and 118 episodes. Episodes of ventricular tachycardia were more numerous in patients with frequent or polymorphic premature ventricular complexes than in patients with sporadic or monomorphic premature ventricular complexes. Fifty-seven ventricular tachycardia episodes were analyzed: 30 of 3 beats, 25 of 4-9 beats and 2 of 15 beats. Forty-seven episodes were monomorphic and 10 (17.5%) were polymorphic. The ventricular tachycardia rate was 136.4 +/- 25 b/m' (range 104-200). The RR'/QT ratio (where RR' = coupling interval of the first beat of ventricular tachycardia) was 1.67 +/- 0.42 and was not correlated either with the rate or the number of beats of ventricular tachycardia. Heart rate at the moment of ventricular tachycardia was 82 +/- 15 b/m' and QT interval 0.36 +/- 0.05 sec; there was no difference when compared to their values of 1 and 5 minutes before ventricular tachycardia. Furthermore, the heart rate showed no difference when compared to the mean value of the hours in which ventricular tachycardia episodes occurred. In addition, heart rate was not correlated with ventricular tachycardia rate, whereas a good correlation was found between the last RR interval preceding ventricular tachycardia and RR' interval (r = 0.61, P less than 0.01).

Aged↗
PubMed1989

[Bidirectional tachycardia during therapy with lorajmine].

We report a case of bidirectional tachycardia (BT) found on Holter recording (H-ECG), likely due to antiarrhythmic therapy with lorajmine. The patient, who was not on digitalis therapy and had good myocardial function, was investigated for presyncope. H-ECG revealed frequent premature ventricular complexes (PVC). Disopyramide, lorajmine and amiodarone (in succession) were ineffective in controlling the arrhythmias. During therapy with lorajmine (600 mg/die) H-ECG showed numerous symptomless episodes of BT. Two forms of BT were found. In the first one the PVC had a right bundle branch block (BBB) pattern in lead CM1 and alternating polarity (Rs-rS) in lead CM5, whereas in the second one an alternating right and left BBB pattern in CM1 was found. PVC were subsequently controlled with flecainide. In a 4-year follow-up period the patient underwent several H-ECGs, both with and without antiarrhythmic drugs; however, BT episodes were found only during lorajmine therapy. Thus, this drug was likely responsible for the appearance of BT episodes.

Aged↗
PubMed1989

Rhythm of carnitine levels in serum and urine of normal subjects.

A study of the diurnal serum and urine levels of L-carnitine and acetylcarnitine was carried out in eleven healthy volunteers. No significant difference was found between the levels in the morning and in the afternoon, although a higher carnitinaemia was shown in the waking hours when the energy demands were higher.

Acetylcarnitine↗
PubMed1988

Circadian variation of ventricular tachycardia in acute myocardial infarction.

Circadian rhythms have been described both for acute myocardial infarction (AMI) and sudden death. In this study the diurnal distribution of ventricular tachycardia (VT) in patients with AMI was analyzed. Ninety-four AMI patients with greater than or equal to 1 VT on Holter electrocardiographic monitoring who were not taking antiarrhythmic drugs were studied. Forty-seven patients had a recent AMI (group A) and 47 an old AMI (group B). Chronobiologic analysis was made by single cosinor method. There were 157 VTs (mean 1.67 VTs/patient, range 1 to 10) in the 94 patients: 70 in group A and 87 in group B. A significant circadian rhythm of VT was found in the total population with acrophase at 2:29 P.M. The hourly distribution of VT showed a tendency to bimodality, which seemed due to a different time of peak VT occurrence in group A (significant rhythm with acrophase at 4:40 P.M.) and group B (significant rhythm with acrophase at 12:39 P.M.). Thus, the hourly VT frequency in patients with AMI has a significant circadian variation with the highest occurrence in the awake hours, similar to the rhythms described for AMI and sudden death.

Aged↗
PubMed1987

Circadian rhythm of ventricular tachycardia.

A 24-hr electrocardiographic monitoring was performed in 406 patients (297 with ischemic heart disease). Forty-one episodes of ventricular tachycardia were detected in 32 subjects (7.88%). The average rate of tachycardia was 127.4 (range 180-65). No correlation was observed between the rate of ventricular tachycardia and the heart rate 30, 20, and 10 min before and at the moment of the episode. A circadian rhythm of all the episodes was demonstrated, with an acrophase at 1102 hr. A different acrophase was observed for the QT interval. No significant rhythm was observed for premature ventricular beats in the patients with ventricular tachycardia. The circadian variation of tachycardia suggests that this arrhythmia is related to sympathetic tone, but it will require further studies with a larger number of patients with ventricular tachycardia to clarify this problem.

Circadian Rhythm↗