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M D Guazzi

Publications and source records attributed to M D Guazzi.

At least 19 recordsLinked to original sources
PubMed1998

Thrombin activation and late restenosis after percutaneous transluminal coronary angioplasty.

BACKGROUND: Mechanisms of restenosis after percutaneous transluminal coronary angioplasty (PTCA) have not been defined yet. Experimental studies have shown that thrombin, by stimulating platelet growth factor secretion and smooth muscle cell proliferation, can play a major role. METHODS AND RESULTS: In 34 patients with single-vessel coronary disease undergoing PTCA, thrombin activity was evaluated through serial fibrinopeptide A (FPA) plasma determinations. Samples were performed before PTCA, immediately after and 24 hours, 72 hours, and 6 months later. Patients were grouped according to the development (group 1, n = 13) or nondevelopment (group 2, n = 21 ) of restenosis at a 6-month angiographic control. No difference in the two groups was found concerning baseline FPA values. In patients in group 1, soon after PTCA higher FPA levels (27.3 +/- 13.7 ng/ml) than those in group 2 (9.2 +/- 5.6 ng/ml; p < 0.05 vs pre-PTCA, and p < 0.01 between the two groups) were observed. No differences in FPA levels were detected at the other steps between the two groups. CONCLUSION: Our data suggest that thrombin plays a role in the process of restenosis after PTCA; acute FPA response to the procedure seems to have a predictive value.

Aged↗
PubMed1998

Antihypertensive efficacy of angiotensin converting enzyme inhibition and aspirin counteraction.

OBJECTIVE: Blockade of bradykinin breakdown and enhancement of prostaglandin release probably participate in the antihypertensive activity of angiotensin converting enzyme (ACE) inhibitors. Cyclooxygenase blockers may attenuate the efficacy of ACE inhibitors by interfering with prostaglandin synthesis, and patients taking aspirin may not benefit from ACE inhibition. This study was designed to evaluate the incidence of the counteractive phenomenon and to define minimal aspirin dosage that causes an antagonistic effect. METHODS: These were 26 patients with mild to moderate hypertension (group 1) and 26 patients with severe untreated primary hypertension (group 2). Enalapril (20 mg twice a day) was used as a single drug in group 1 and was added to the combination of long-acting nifedipine (30 mg/day) and atenolol (50 mg/day) in group 2. Aspirin was tested at doses of 100 and 300 mg/day, and an attenuation of more than 20% of the mean blood pressure decrease produced by enalapril was the criteria that defined antagonism. RESULTS: The 100 mg dose was ineffective. However, 300 mg aspirin had an antagonistic effect in 57% of patients in group 1 and 50% of patients in group 2: mean arterial pressure was lowered by 63% and 91% less, respectively. Results were independent of the drug administration order. In "responders," aspirin significantly attenuated the renin rise associated with ACE inhibition. CONCLUSIONS: These findings suggest that a number of ACE-inhibited patients are susceptible to 300 mg/day aspirin, regardless of hypertension severity. Antagonism may be mediated through prostaglandin inhibition according to predominance, in an individual patient, of prostaglandin activation (also as a renin secretory stimulus) or angiotensin blockade by enalapril.

Adult↗
PubMed1998

[Early evaluation of results from systemic thrombolysis in acute myocardial infarct: the value of troponin I].

Cardiac troponin-T (Tn-T) and troponin I (Tn-I) isoforms are sensitive and specific tests for the diagnosis of acute myocardial infarction. Information is scanty regarding the ability of these markers to discriminate patients with or without reperfusion early after thrombolytic treatment. To this purpose, 64 patients (mean age 63.7 +/- 7.5 years) with acute myocardial infarction, treated with recombinant tissue-type plasminogen activator within 6 hours from the onset of symptoms, were enrolled in the study. Tn-I was determined by immunofluorescency (Dade, Stratus II) at the beginning of thrombolysis, 30 min after therapy (120 min after starting) and every 6 hours in the first 2 days of acute myocardial infarction. At the same intervals, samples for Tn-T (immunoenzymatic methods ELISA), creatin phosphokinase (CK) and CK-MB (biochemical method) were collected. Normal subjects showed values of Tn-I and Tn-T steadily lower than 0.2 micrograms/l. To evaluate reperfusion, for each parameter the time to peak concentration and the ratio (delta) between the levels of the marker 30 min after thrombolysis vs basal, were considered. Coronary angiography was performed in all patients within 4 days, in 48 patients (Group 1) reperfusion (TIMI grade 2-3) of the involved vessel was reached, in 16 (Group 2) reperfusion was absent (TIMI 0-1). In Group 1, at 30 min after the end of thrombolysis, an increase of cardiac Tn-1 of at least 5.5 times compared to baseline, was observed; In-T, CK and CK-MB reached concentrations at least 7-fold greater than basal ones; in Group 2 patients, no significant variation of concentration of all markers was found. Therefore, in order to discriminate between reperfused and non reperfused patients, cut-off values of the ratio delta of 5.5 for Tn-I and of 7 for Tn-T were chosen. By this method, sensitivity for detection of reperfusion was 95, 80, 54 and 56%; specifically 100, 89, 79 and 82%, respectively. In Group 1 Tn-I peaked earlier than other parameters (9.2 +/- 1.7 vs 12.4 +/- 2.4 hours for Tn-T, p< 0.04 and vs 13 +/- 1.7 hours for CK and CK-MB, p<0.03); the peak of each marker showed the following values of sensitivity and specificity for reperfusion: 86 and 89% for Tn-I, 79 and 82% for Tn-T, 78 and 80% for CK, 83 and 80% for CK-MB. The time to peak of troponins, CK and CK-MB is a sensitive index of reperfusion after thrombolytic therapy in acute myocardial infarction; the delta Tn-I is the earliest marker of reperfusion allowing the assessment of efficacy of treatment within 2 hours after its beginning.

Adult↗
PubMed1997

Evidence of multifocal activity of coronary disease in patients with acute myocardial infarction.

BACKGROUND: Destabilization of the fibrous cap facilitates plaque rupture, thrombus formation, and myocardial infarction. Because systemic stimuli, such as lipoproteins, infectious agents, and autoantigens, may incite this reaction, one may wonder whether disruption mechanisms are only local or systemic and infarction is caused by an arbitrary plaque event or by a systemic, acute activity of the coronary disease. METHODS AND RESULTS: Early (3 to 5 days) and late (1 month) peri-infarction coronary angiographic data in 23 patients with first infarction were compared with that in 23 similar patients, with angiography performed because of stable angina and repeated after 1 month before angioplasty. Nonculprit lesion changes at the narrowest point defined progression or regression when exceeding 0.27 mm. In patients with recent infarction we found that 16 had progression, 4 had regression, 1 had both, 2 were steady (values in patients with stable angina being 2 [P<.0011, 1 [NS], 0 [NS], and 20 [P<.001]); 27 lesions were infarct related; 17 of the 45 nonculprit lesions progressed and 5 regressed (values in stable angina being 2 [P<.001] and 1 [P<.05] out of 78); minimal diameter reduction of progressing stenoses averaged 0.39 mm; lumen increase of regressing lesions averaged 0.30 mm; 3 patients developed interim rest angina associated with progression of a nonculprit lesion. CONCLUSIONS: A greater proportion of subjects and lesions with progression or regression (in infarction versus stable angina) supports the hypothesis that infarction is a hallmark of systemic coronary disease activity. Changes might vary according to the "maturation" stage of an atheroma, and maximal expression would be at the level of the offending plaque. Shrinkage, thrombolysis, or vascular remodeling would determine the residual plaque morphology.

Analysis of Variance↗
PubMed1996

Reversal of heart failure with sotalol in a case of incessant supraventricular tachycardia.

Supraventricular tachycardia inducing severe left ventricular enlargement and dysfunction was treated with sotalol in a 17-year-old man, in whom radiofrequency ablation had been unsuccessful. Restoration of sinus rhythm overwhelmed the negative inotropic effect of the drug and caused full reversion to normal of the left ventricular dimensions and function.

Adolescent↗
PubMed1996

Treatment of ostial lesions of the left anterior descending coronary artery with Palmaz-Schatz coronary stent.

We evaluated acute and long-term clinical and angiographic results of elective Palmaz-Schatz coronary stent implantation for left anterior descending coronary artery (LAD) ostial stenosis in 23 consecutive patients. Eight patients had stable angina, 14 had unstable angina, and 1 had recent myocardial infarction. Sixteen patients had single-vessel, 5 had double-vessel, and 2 had triple-vessel disease. Clinical success without major complications (death, acute myocardial infarction, emergency coronary artery bypass grafting) was obtained in all cases and technical success in 20 cases (86.9%). After stenting, minimal lumen diameter increased from 1.05 +/- 0.45 mm to 2.89 +/- 0.52 mm (p < 0.001), and percent diameter stenosis decreased from 65.49% +/- 13.36% to 2.94% +/- 19.93% (p < 0.001). One case of subacute thrombosis and no major bleeding occurred. Twenty patients were followed-up for 6 months, during which no acute cardiac event (death, acute myocardial infarction) was observed. Eighteen patients were eligible for follow-up coronary angiography; restenosis (> or = 50% diameter stenosis) was observed in 4 (22.2%). Minimal lumen diameter was 1.77 +/- 0.55 mm, percent diameter stenosis was 39.66% +/- 17.62%, late loss was 1.01 +/- 0.69 mm, net gain was 0.79 +/- 0.55 mm, and loss index (late loss/acute gain) was 0.53 +/- 0.37. This study suggests that elective Palmaz-Schatz stent implantation may be a safe and successful treatment of LAD ostial lesions and provides a large increase in lumen diameter.

Angioplasty, Balloon, Coronary↗
PubMed1996

Late activation of the fibrinolytic system in myocardial infarction treated with thrombolytic therapy. Influence of the coronary anatomical substrate.

Procoagulant activity, thrombin and fibrinolytic system activation have been demonstrated in the first 24-48 h after acute myocardial infarction treated with thrombolytic therapy. Little is known about what happens in the subsequent days, during which the incidence of ischaemic recurrence is high. In 21 patients treated with streptokinase and in 20 patients treated with urokinase we evaluated, with multiple plasma determinations, D-dimer and fibrinogen plasma levels in the first week after myocardial infarction. From the 2nd hour after the beginning of thrombolysis to the 4th day, all patients received intravenous heparin in doses sufficient to raise the partial thromboplastin time to twice its normal level; subcutaneous calcium heparin (12,000 U/day) was subsequently substituted for the intravenous route. Coronary angiography was performed 7 days after infarction. From the basal values 2.22 +/- 1.44 nmol.1(-1) in the streptokinase group and 3.28 +/- 3.05 nmol.1(-1) in the urokinase group, D-dimer rose consistently in the 1st hour after thrombolysis 269.4 +/- 206.7 nmol.1(-1) and 44.5 +/- 35.5 nmol.1(-1) in the streptokinase and urokinase groups, respectively; P < 0.001. After the peak value, which in both groups was reached after 5 h, D-dimer slowly decreased during the study period. It reverted to normal values only in 10/21 patients in the streptokinase group; in the urokinase group normalization was attained in 14/20 patients between the 3rd and 6th days. After withdrawal of i.v. heparin in patients of both groups with TIMI 0 or 1 grade of coronary patency, D-dimer rose to levels four to seven times greater than normal; in patients of both groups with TIMI 2 or 3 grade coronary flow, D-dimer showed a monophasic pattern of progressive normalization (P < 0.05 and P < 0.01 at the 6th and 7th days, respectively, for differences between TIMI 0-1 and TIMI 2-3 groups). After myocardial infarction, thrombolysis is followed by active and persistent fibrin degradation more marked and lasting after streptokinase than after urokinase. When occurring sooner, it is a consequence of plasmin activation induced by thrombolytic agents; later it seems to be related to intracoronary substrate, as suggested by the relationship of plasma elevation of D-dimer with the presence of occluded or suboccluded infarction-related vessels.

Aged↗
PubMed1996

[Ejection fraction].

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Cardiovascular Diseases↗
PubMed1996

Valve design characteristics and cine-fluoroscopic appearance of five currently available bileaflet prosthetic heart valves.

Bileaflet prostheses are low profile, central flow orifice devices that show excellent hemodynamic performance and low thrombogenicity. Five models are currently used for heart valve replacement. Comprehensive and comparative studies regarding valve characteristics and functioning are lacking, making the updating and the familiarization by physicians and cardiologists with these prostheses difficult. We describe the valve design characteristics and evaluate the cine-fluoroscopic appearance and functioning of 387 bileaflet prostheses that have been implanted in 367 consecutive patients. The valve types are St Jude Medical (n = 69), Edwards-Duromedics (n = 74), Carbomedics (n = 1290) Sorin Bicarbon (n = 88) and Jyros (n = 27). The prostheses' fluoroscopic appearance was evaluated through multiple radiographic views (Siemens-Elema equipment with C-arm); the prostheses' functional evaluation was performed by obtaining the "tilting disk projection" (ie, with the radiographic beam parallel to both the valve ring plane and the tilting axis of disks) to calculate opening, closing, and travel angles of the disks. This study shows that each of the five bileaflet valves has distinctive design characteristics. Fluoroscopy is an easy, readily available, and useful technique that correctly identifies the prosthesis type and properly evaluates its functioning in the majority of cases.

Aortic Valve↗
PubMed1996

Fluoroscopic functional evaluation of bileaflet prostheses: effect of different intraoperative valve orientation.

Fluoroscopy is a reliable, easy, and readily available technique to follow-up prosthesis functioning after heart valve surgery. The different orientation given to the prosthesis may represent a limitation of the technique accounting for unsatisfactory results in 10% to 40% of the cases. The aim of the study was to evaluate whether and to what extent different intraoperative valve orientation influence feasibility and accuracy of postoperative fluoroscopic evaluation of bileaflet prostheses. We prospectively evaluated 90 patients who had aortic, mitral, and/or tricuspid valve replacement with Sorin Bicarbon or CarboMedics bileaflet prostheses. Fifty percent of the patients in each group were randomly assigned to receive prostheses oriented in a perpendicular or a parallel position with respect to the ventricular septum. Fluoroscopic evaluation was considered appropriate when the prosthesis' "tilting disk" projection was obtained. The valve's hemodynamic performance was investigated through Doppler study. A proper fluoroscopic evaluation was rapidly (15 +/- 5 seconds) achieved in all patients with the former orientation, whereas it was impossible to obtain it in 8 of 20 (40%), 19 of 20 (95%), and 4 of 5 (80%) of patients with the latter orientation. In the remaining patients extremely angulated, uneasy projection was often required to get a correct fluoroscopic image. The Doppler study showed a similarly favorable hemodynamic performance regardless of valve orientation. Prosthesis orientation crucially affects the rate of success of the fluoroscopic evaluation. The orientation perpendicular to the ventricular septum greatly facilitates the postoperative feasibility and accuracy of fluoroscopy, and it is not detrimental to the valve's hemodynamic performance. This valve orientation may provide a better fluoroscopic window whenever a valve dysfunction is suspected.

Aortic Valve↗