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Biomedical subjects

P Zardini

Publications and source records attributed to P Zardini.

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

Acute anterior myocardial infarction: increased dye intensity in the myocardial risk area after coronary angioplasty is associated with reduction of diastolic volumes.

BACKGROUND: Myocardial perfusion in the risk area during the acute phase of myocardial infarction has been extensively investigated over the last few years. The so-called "no-reflow" or "low-reflow phenomenon" (absence of myocardial perfusion despite patency of the infarct-related coronary artery) was shown to correlate with worse postinfarction remodeling, in particular when myocardial contrast echocardiography was used. The aim of this study was to determine, during routine coronary angiography performed before and after coronary angioplasty (PTCA) during the acute phase of myocardial infarction, the existence of the no-reflow phenomenon and its relation with ventricular remodeling, by evaluating the dye video density in the myocardial risk area. This confirmation by a different diagnostic technique may serve to highlight the role of myocardial perfusion as an index of prognosis in the clinical setting of acute myocardial infarction. METHODS: Twenty-six patients (23 males, 3 females, mean age 57 +/- 8.7 years) who underwent either rescue (n = 11, 42.3%) or primary PTCA, according to clinical indications, of the left anterior descending coronary artery during an acute anterior myocardial infarction and who did not have stenosis of the left circumflex or right coronary artery, were retrospectively selected from a 6 year intake. The extent of coronary stenosis was assessed using biplane quantitative coronary angiography, while end-diastolic and end-systolic volume indexes, together with regional wall motion, were computed from echocardiography performed in the first 24 hours and at 6 months. Patients were subdivided into two groups on the basis of dye video intensity in the risk area, as assessed from images obtained during left main coronary artery injections before and immediately after PTCA. It was used a subtraction technique (Group A: increased video intensity, n = 12; Group B: no change, n = 14), assuming that higher peak intensity reflects greater myocardial blood volume. Three patients in Group B with ineffective PTCA were excluded, so that the final number of considered patients was 11. RESULTS: The distribution of rescue PTCA was similar in the two groups (7 in Group A vs 3 in Group B, p = 0.13) as were clinical characteristics and therapeutic regimen. There was a significant time * group interaction for end-diastolic volumes (-4.6 +/- 23% in Group A vs +22 +/- 22% in Group B, p = 0.029), whereas end-systolic volumes showed a tendency to greater dilation in Group B (+19 +/- 28% vs +0.9 +/- 31% in Group A), although this difference was not significant (p = 0.27). No interaction was evident for increase in the vessel area (+46 +/- 12.5% in Group A vs +43.2 +/- 13.6% in Group B, p = 0.99), or for extent of regional dysfunction (+3.08 +/- 10.9 chords in Group A vs -2.5 +/- 9.5 chords in Group B, p = 0.50). CONCLUSIONS: The detection of myocardial blood volume in the risk area using dye video intensity during left main dye contrast injection, is useful to distinguish whether there is improved perfusion at the muscular level, following successful angioplasty of the infarct-related coronary artery. Lack of improved myocardial perfusion has an adverse effect on left ventricular volumes independently of coronary stenosis resolution and regional wall motion changes in the time.

Aged↗
PubMed1999

The extent of regional wall motion abnormalities identifies patients at risk of extensive left ventricular remodeling: implications for the design of post myocardial infarction trials.

BACKGROUND: The FAMIS (Fosinopril in Acute Myocardial Infarction Study) was a multicenter, placebo-controlled, double-blind trial designed to evaluate the safety and the efficacy of fosinopril in reducing left ventricular enlargement after acute anterior myocardial infarction. We evaluated the echocardiographic examinations performed during the trial in order to assess the trend of the remodeling process over time and to evaluate the role of infarct size in identifying patients at risk of progressive left ventricular dilation. METHODS: A complete echocardiographic examination was performed on admission, before discharge and three months later. Patients undergoing coronary bypass surgery or PTCA had a further examination prior to the procedure. The echocardiograms were analyzed at a central laboratory, and the end-diastolic and end-systolic left ventricular volumes were computed by using a modified Simpson's rule technique. Regional wall motion was evaluated using the centerline method, analyzing the left ventricular boundary along 100 chords perpendicular to the centerline constructed midway between the end-diastolic and the end-systolic contours. A quantitative infarct-size index was then computed according to the number of chords with a fractional shortening equal to or less than 5%. RESULTS: Left ventricular end-diastolic and end-systolic volume index significantly increased over time (p < 0.0001); as a result, the stroke volume increased (p < 0.0001) but the ejection fraction did not change. Patients were then divided according to the three-month infarct-size index. For both end-diastolic and end-systolic volume, not only did larger infarcts had higher volumes, but there was also a greater increase from baseline to 3 months. Moreover, larger infarcts had a lower ejection fraction, with a further reduction over the three months, while smaller infarcts had higher values and an increase over time. An infarct-size index of 25 or larger allowed prospective identification at the baseline examination of patients at risk of subsequent left ventricular dilation. CONCLUSIONS: In conclusion, patients at greatest risk of left ventricular dilation, namely those with larger infarct size, constitute a group that is worth considering for any therapeutic effort for reducing the remodeling process. These patients could in fact benefit from therapeutic strategies aimed at the reduction of left ventricular remodeling and should be studied in clinical trials.

Aged↗
PubMed1998

Increased intensity of contrast material immediately after late angioplasty of infarct-related coronary artery is associated with reduced ventricular volumes at six months.

To assess the contribution of residual muscle perfusion in the infarcted territory to prevent ventricular remodeling, 24 patients with 1-vessel disease underwent coronary angiography and angioplasty of a critical left anterior descending coronary stenosis 18+/-11 days after a first anterior myocardial infarction. The degree of stenosis was assessed using biplane quantitative angiography, whereas ventricular volumes, together with regional wall motion, were computed from single-plane ventriculography. Patients were reevaluated at 6 months after they had been subdivided according to the videointensity of the territory of the culprit vessel, as assessed from images obtained during main stem dye contrast injections before and immediately after angioplasty using a subtraction technique (group A, increased intensity [n= 15]; group B, no change [n=9]), assuming that higher peak intensities reflect greater myocardial blood volume. There was a significant time group interaction for ventricular volumes (diastolic, -13+/-12% for group A vs +20+/-24% for group B, p=0.008; systolic, -15+/-19% for group A vs +18+/-36% for group B, p=0.017), although no interaction was evident for the degree of resolution of coronary stenosis or the extent of recovery of regional dysfunction. The effects on volumes were paralleled by changes in ventricular end-diastolic pressure (-3+/-7 mm Hg in group A vs +5+/-6 mm Hg in group B, p=0.006), although baseline clinical characteristics and medical regimen over the 6-month period were quite comparable between the 2 groups. In conclusion, despite late angioplasty of the culprit vessel, ventricular remodeling is prevented mainly when the procedure guarantees improved perfusion at the muscular level. The result is not necessarily mediated by recovery of regional systolic function.

Aged↗
PubMed1998

Increasing degrees of left ventricular filling impairment modulate left atrial function in humans.

We sought to investigate the changes in atrial reservoir, pump, and conduit functions that are associated with increasing degrees of left ventricular filling impairment. In 13 patients with an impaired relaxation type of filling and in 15 with restrictive patterns, the left atrial volume curve was constructed combining Doppler and 2-dimensional echocardiography. Nine normal subjects served as controls. Left atrial reservoir (defined as [maximum - minimum atrial volume] minus the amount of blood flow reversal in the pulmonary veins with atrial contraction), pump (defined by the volume of blood that enters the ventricle with atrial contraction), and conduit functions (defined as left ventricular filling volume - [left atrial reservoir plus pump volume]) were computed and each expressed as a percentage of ventricular filling volume. The atrial reservoir function was higher in the impaired relaxation group than in normal subjects (49+/-8% vs 38+/-8%, p <0.01) but markedly lower in the restrictive group (27+/-8%, p <0.05). The reverse was true for conduit function, exaggerated in restrictive group (54+/-12% vs 36+/-11% in normal subjects, p <0.01) but minimized in patients with an impaired relaxation type of filling (14+/-9%, p <0.001). The atrial pump contributed 19+/-6% of ventricular filling volume in restrictives, 26+/-3% in normals (p <0.01), and 38+/-4% (p <0.001) in the impaired relaxation group. We conclude that increased atrial response to early-stage left ventricular filling impairment is characterized by augmented reservoir and pump functions, according to a Starling mechanism, which becomes hardly effective at end-stage ventricular dysfunction when the limits of the atrial preload reserve are reached. At this stage, conduit in the atrium takes precedence.

Adult↗
PubMed1998

Prognostic value of detection of myocardial viability using low-dose dobutamine echocardiography in infarcted patients.

Revascularization can improve ventricular function in patients with viable myocardium, but whether and how the presence of viable myocardium affects prognosis of infarcted patients is still far from clear. Thus, 202 patients (173 men, 59 +/- 9 years old) with a previous or recent myocardial infarction (MI) and regional asynergies underwent low-dose dobutamine echocardiography (5-15 microg/kg per min) to assess myocardial viability and were followed for a period of 16 +/- 11 months after revascularization (89 patients) or medical therapy (113 patients). Four groups of patients were defined: (1) patients with viability, revascularized (n = 64); (2) patients with viability, treated medically (n = 52); (3) patients without viability, revascularized (n = 25); and (4) patients without viability, treated medically (n = 61). Of these patients, 45 (23%) patients suffered 57 cardiac events: 18 cardiac deaths (9%), 7 MIs, 12 unstable angina, 9 heart failures, and 11 new revascularization procedures. Patients with viability, revascularized, experienced a slightly lower event rate (22%) compared with patients with viability, treated medically, patients without viability, treated medically and patients without viability, revascularized (29%, 31%, and 36%, respectively; p = not significant [NS]). The frequency of events was then evaluated in those 108 patients with an ejection fraction < or =33%, in whom 14 cardiac deaths occurred: the incidence of cardiac death was slightly lower in patients with viability, revascularized (3/37, 8%) than in the patients with viability, treated medically (4/26, 15%), patients without viability, revascularized (2/11, 18%), or patients without viability, treated medically (5/34, 15%) (p = NS). Nonfatal cardiac events were significantly fewer (p <0.05) in patients with viability, revascularized (8%) and in patients without viability, treated medically (6%) than in patients with viability, treated medically and patients without viability, revascularized (27%). In infarcted patients with severe left ventricular dysfunction, the presence of viable myocardium, if left unrevascularized, leads to further events. On the contrary, in the absence of myocardial viability, revascularization could lead to a worse prognosis than medical therapy.

Aged↗
PubMed1998

Short- and long-term effects of early fosinopril administration in patients with acute anterior myocardial infarction undergoing intravenous thrombolysis: results from the Fosinopril in Acute Myocardial Infarction Study. FAMIS Working Party.

BACKGROUND: Angiotensin-converting enzyme inhibitors are used in patients who have myocardial infarction with left ventricular (LV) dysfunction. Few data are available in patients whose LV function is within the normal range. METHODS AND RESULTS: The Fosinopril in Acute Myocardial Infarction Study was a 2-year, randomized, double-blind, placebo-controlled, multicenter study of 285 patients with anterior acute myocardial infarction and was designed to investigate the effects of the early (<9 hours) administration of fosinopril and thrombolysis on (1) changes in echocardiographically evaluated LV volumes at 3 months and (2) long-term occurrence of death and congestive heart failure. LV volumes were normal at baseline in more than 70% of patients and were comparable between groups both at baseline and after 3 months of treatment. Fosinopril-treated patients showed a 30% reduction in the 2-year combined prevalence of death or moderate-to-severe congestive heart failure (New York Heart Association class III-IV) despite having a worse clinical profile at baseline. The benefit of fosinopril was confirmed both in patients without congestive heart failure at admission and in those with ejection fraction >40% at baseline. Moreover, the incidence of significant ventricular arrhythmias was lower in the fosinopril group (0.8% vs 6.0%, p < 0.02). CONCLUSIONS: The results of the Fosinopril in Acute Myocardial Infarction Study suggest that early treatment with fosinopril can benefit patients with acute myocardial infarction in addition to a prevention of LV remodeling.

Aged↗
PubMed1997

Comparison of left ventricular function and volumes during transesophageal atrial pacing combined with two-dimensional echocardiography in patients with syndrome X, atherosclerotic coronary artery disease, and normal subjects.

Nine patients with syndrome X were compared with 2 groups of patients known to have coronary artery disease (CAD) (8 patients who developed regional wall motion abnormalities [group ECHO+] and 6 patients who showed only ST depression at echo-pacing [group ECG+]) and with 6 healthy volunteer control subjects. Left ventricular function at rest was normal in all patients. End-diastolic and end-systolic volumes (ml/m2) and ejection fraction were calculated at baseline and at peak of echo-pacing using a Simpson's biplane method. No regional wall motion abnormalities were observed during the echo-pacing in patients with syndrome X or in the volunteers. End-diastolic volume decreased in patients with syndrome X, in the volunteers (from 47 +/- 11 to 30 +/- 12 and from 72 +/- 7 to 38 +/- 6, respectively, p <0.01 for both), and in ECG+ patients (from 48 +/- 10 to 33 +/- 6, p <0.05), whereas it did not change in ECHO+ patients. End-systolic volume decreased in patients with syndrome X and in the volunteers (from 17 +/- 5 to 11 +/- 4 and from 28 +/- 6 to 16 +/- 4, respectively, p <0.01 for both), whereas it did not change or else slightly increased in patients with CAD (from 18 +/- 10 to 16 +/- 5 for ECG+ patients and from 19 +/- 5 to 24 +/- 9 for ECHO+ patients, p = NS for both), regardless of whether regional wall motion abnormalities appeared. Ejection fraction decreased in ECG+ and ECHO+ patients (from 64 +/- 12 to 52 +/- 11 and from 62 +/- 9 to 44 +/- 13, respectively, p <0.01 for both), whereas it did not change in patients with syndrome X and in the volunteers (from 64 +/- 8 to 61 +/- 8 and from 61 +/- 7 to 58 +/- 7, respectively, p = NS for both). During echo-pacing in syndrome X patients no regional wall motion was detected. Left ventricular volumes and ejection fraction showed the same patterns of variation in these patients as they did in the healthy control subjects, in contrast with those patients with CAD, whether or not regional wall motion abnormalities appeared in the latter.

Aged↗
PubMed1997

Opposite effects of the remodeling of infarcted and non-infarcted myocardium on left ventricular function early after infarction in humans. An echocardiographic study in patients examined before and after myocardial infarction.

OBJECTIVE: The purpose of this study was to evaluate infarction-related changes in the infarcted and the non-infarcted myocardium using a baseline assessment of ventricular function obtained prior to the infarction. BACKGROUND: Experimental studies have shown that both infarcted and non-infarcted myocardium contribute to the process of left ventricular dilatation soon after the infarction, but no data exist on the effect that the infarct has on the pre-infarct ventricular morphology in humans. METHODS AND RESULTS: 10 patients, out of 721 admitted to our coronary care unit with a first acute myocardial infarction over a 3-year period, had had an echocardiographic examination performed before (354 +/- 407 days) and after (10 +/- 9 days) the infarction which were adequate for quantitative evaluation. Ventricular volume (Simpson) and regional wall motion (Centerline method) were evaluated by biplane apical sections and the endocardial length of the infarct and the non-infarct segments, imaged in a cross-sectional view at the papillary muscle level, were measured. After the infarction end-diastolic and end-systolic ventricular volume increased (P = 0.0003 and P < 0.0001, respectively); diastolic and systolic infarct segment length increased (P = 0.011 and P = 0.0008, respectively), while non-infarct segment had only diastolic lengthening (P = 0.019), without systolic changes. The ejection fraction decreased after the infarction (P < 0.0001), in inverse relation to infarct size and in direct relation to diastolic non-infarct segment lengthening. In the five patients in whom there was a significant diastolic lengthening of non-infarct segment (larger than mean +/- 2 S.D. of the interobserver variability) the decrease in ejection fraction was less than in the patients without significant lengthening of this segment (P = 0.017), despite a similar echocardiographic infarct size index. CONCLUSION: Ventricular enlargement early after myocardial infarction is due to both infarct expansion and lengthening of non-infarct segment. However, while systolic stretching of the infarct segment is a deleterious process that accounts for the increase in end-systolic volume, diastolic non-infarct segment lengthening is the expression of a functional compensatory mechanism that counteracts the reduction of the ventricular pump function secondary to the infarction.

Aged↗
PubMed1997

Post acute myocardial infarction: the Fosinopril in Acute Myocardial Infarction Study (FAMIS).

Many studies have clearly documented the beneficial effects of angiotensin converting enzyme (ACE) inhibitors in patients with acute myocardial infarction (AMI). The Fosinopril in Acute Myocardial Infarction Study (FAMIS) was a 2-year randomized, double-blind, placebo-controlled multicenter study investigating the hemodynamic and clinical effects of early (< 9 h from onset of symptoms) administration of fosinopril in 285 patients with anterior AMI undergoing thrombolysis within 6 h of symptom onset. The objective of the study was twofold: 1) to estimate changes in left ventricular (LV) volumes and function over 3 months by a series of echocardiographic evaluations, and 2) to clinically assess mortality and the occurrence of congestive heart failure (CHF) over 2 years. LV volumes measured at baseline (24 to 48 h from symptom onset) were within the normal range in over two-thirds of randomized patients, and the changes in volume were comparable after 3 months of treatment with either fosinopril or placebo. However, fosinopril-treated patients showed a 30% reduction in the 2-year incidence of death or moderate-to-severe CHF (P = .04) despite having a worst prognostic profile at baseline. This benefit of fosinopril was confirmed in the subgroup of patients without CHF on admission, who showed a 34.1% reduction in the 2-year occurrence of CHF (P = .05) and a 29.1% reduction in death or CHF (P = .04). The results of the FAMIS study suggest that early treatment with fosinopril, in conjunction with thrombolysis, can significantly delay the development of CHF in patients with AMI, acting through mechanisms independent of fosinopril's impact on LV remodeling.

Adolescent↗
PubMed1997

Lisinopril in the treatment of congestive heart failure in elderly patients: comparison versus captopril.

The present study was performed in order to compare the efficacy, safety, and tolerability of lisinopril, a long-acting angiotensin-converting enzyme (ACE) inhibitor, with captopril, the shorter acting ACE inhibitor available, in the treatment of elderly patients (mean age 70 +/- 0.5 years) with congestive heart failure (mean left ventricular ejection fraction 33.5 +/- 1%). The study was organized according to a double-blind, parallel-group, randomized multicenter protocol. After a 14-day placebo run-in period, patients were randomized to receive either lisinopril 5 mg orally once per day or captopril 12.5 mg orally once per day. The dose of the study drug could be doubled at 2-week intervals for 6 weeks. The maximal dose was lisinopril 20 mg once per day or captopril 25 mg twice per day. The addition of either captopril or lisinopril to a regimen of diuretics caused a significant increase in exercise tolerance assessed by bicycle ergometry after 12 weeks of treatment (530 +/- 21 seconds vs. 431 +/- 13 seconds, p < 0.01; 555 +/- 19 seconds vs. 463 +/- 12 seconds, p < 0.01, respectively). Both drugs significantly increased left ventricular ejection fraction and stroke volume, were equally effective in improving NYHA class, and were well tolerated, with no differences detectable between treatments. The results of this study indicate that lisinopril 5-20 mg once daily is at least as effective and well tolerated as captopril 12.5-50 mg daily in the treatment of elderly patients with congestive heart failure.

Aged↗
PubMed1997

Does prostaglandin E1 infusion affect the left ventricular filling pattern of end-stage dilated cardiomyopathy? A combined hemodynamic-echo Doppler study.

Prostaglandin E1 improves hemodynamics in patients with severe dilated cardiomyopathy and pulmonary hypertension through it's reducing action on pulmonary resistances. However, few data are available to indicate whether these beneficial effects on right heart hemodynamics translate into any improvement of the altered left ventricular filling pattern that characterizes this condition. We studied 12 patients with dilated cardiomyopathy during preoperative evaluation for cardiac transplantation before and after prostaglandin E1, 30-50 ng/kg/min i.v. Patients underwent catheterization of the right heart and left ventricle by Swan-Ganz catheter, giving simultaneous assessment of pressure by micromanometer and of volume derived from two-dimensional echo-guided Doppler mitral flow velocity, where volume equals mitral velocity integral x valvular area. Prostaglandin E1 induced a significant reduction in mean pulmonary (from 38 to 30 mm Hg; p = 0.0001) and aortic (from 79 to 75 mm Hg, p = 0.05) pressures but no change in heart rate or tau. Peak A wave increased from 28 to 33 cm/s (p = 0.02), along with a reduction in end-diastolic pressure from 29 to 26 mm Hg (p < 0.04), whereas peak E wave did not change. E/A ratio decreased slightly (from 2.5 to 2.1; p < 0.0007) but did not reverse. Systolic volumes decreased (from 231 to 212 ml; p < 0.05), and cardiac index increased from 2.1 to 2.6 L/min/m2 (p = 0.0002) because of a reduction in pulmonary and systemic vascular resistances. The diastolic pressure-volume relation shifted downward along the same curve. Prostaglandin E1 infusion in patients with severe dilated cardiomyopathy and pulmonary hypertension reduces pulmonary and systemic resistances without affecting heart rate, relaxation, or passive diastolic left ventricular properties. Systolic right and left ventricular unloading increases cardiac index, facilitating ventricular emptying. E/A ratio does not reverse, although it decreases slightly, with mechanisms, however, that appear independent of any direct effect of the drug on the ventricular diastolic properties.

Alprostadil↗