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R Zeppellini

Publications and source records attributed to R Zeppellini.

At least 19 recordsLinked to original sources
PubMed2004

Early and subtle abnormalities of left ventricular function in clinically stable coronary artery disease patients with normal ejection fraction.

BACKGROUND: It has been reported that, in the initial phase of ischemic cardiomyopathy, the earliest alterations of left ventricular function are detected during the relaxation phase. The aim of this study was to look for precocious abnormalities in the early stage of ischemic cardiomyopathy in both left ventricular systolic and diastolic phases. METHODS AND RESULTS: Using simultaneous left ventricular catheterization and echo-Doppler techniques, we studied both systolic and diastolic function in 44 (37 males and 7 females, mean age 55.7+/-8) normotensive, clinically stable, coronary artery disease patients with normal left ventricular ejection fraction in comparison to 9 age- and sex-matched normal control subjects (7 males and 2 females, mean age 54.7+/-9). Mean values of E deceleration time, tau, left ventricular end-diastolic volume and pressure, and end-systolic volume and lowest diastolic pressure were significantly higher (from P<.05 to P<.01), whereas mean dP/dt/P values significantly lower (P<.05) in coronary artery disease patients than in controls. A strict relationship (P<.001) between dP/dt/P and tau, left ventricular lowest and end-diastolic pressure was found in all subjects studied. CONCLUSION: Early and subtle abnormalities in parameters of both systolic and diastolic function can be found in the majority of coronary artery disease patients with normal ejection fraction.

Coronary Artery Disease↗
PubMed2001

Detection of early abnormalities of left ventricular function by hemodynamic, echo-tissue Doppler imaging, and mitral Doppler flow techniques in patients with coronary artery disease and normal ejection fraction.

We have investigated the possibility of detecting early abnormalities of left ventricular function at the initial phase of ischemic cardiomyopathy. Sixteen normotensive patients with coronary artery disease and normal left ventricular ejection fraction and 6 control patients were studied by invasive hemodynamic techniques in combination with transmitral Doppler flow or with echo-tissue Doppler imaging. The extent of the percentage of left ventricular longitudinal shortening and the systolic peak velocity at echo-tissue Doppler were significantly higher in the control patients than in patients with ischemic cardiomyopathy (P <.01). Left ventricular end-diastolic pressure was higher (P <.05), whereas mean values of isovolumic contraction and relaxation indexes (dP/dt/P: P <.05; +dP/dt: P <.05; -dP/dt: P <.01) were lower in patients with ischemic cardiomyopathy. Tau was significantly longer in ischemic patients (42.7 +/- 8.8 versus 34.5 +/- 3.7 ms, P <.05). In the control patients, the aortic valve closure to peak E interval by transmitral Doppler flow was significantly longer than that measured by echo-tissue Doppler (P <.001), whereas in patients with ischemic cardiomyopathy, this interval difference was still present and significantly shorter (P <.05). In patients with coronary artery disease and normal ejection fraction, minor and early abnormalities of left ventricular function related to isovolumic contraction and relaxation as well as to longitudinal shortening could be detected. In addition, a suction-like effect, detected during early filling evaluation with echo-tissue Doppler, is significantly decreased but not abolished during the early stages of coronary artery disease.

Adult↗
PubMed1999

C-reactive protein on admission as a predictor of in-hospital death in the elderly with acute myocardial infarction.

BACKGROUND: The mean age of patients with acute myocardial infarction is increasing and the associated in-hospital mortality is exponentially age-related. Inflammation markers have been related to cardiovascular short and long-term prognosis. The aim of this study was to evaluate the short-term prognostic value of C-reactive protein (CRP) levels on admission in the oldest segment of the patients with acute myocardial infarction. METHODS: CRP was prospectively measured on admission by immunonephelometry in 205 consecutive old women (mean age 82 +/- 5 years) with definite acute myocardial infarction; values were then related to in-hospital mortality and the causes of death. RESULTS: CRP levels ranged from 0.1 to 31.9 mg/dl and were raised in 71% of the patients. It showed no significant correlation with baseline clinical variables such as age, history of diabetes or hypertension or prior myocardial infarction, infarct location, and time from symptom onset to admission. The overall in-hospital mortality rate was 25% and rose from 15% among patients in the lower three quartiles of CRP levels (cut point 6.4 mg/dl) to 55% among those in the upper quartile (p < 0.001). By univariate logistic-regression, the odds ratio for early death was 0.84 (95% confidence interval 0.78-0.89) for every increase by 1 mg/dl of CRP, and 5.7 (95% confidence interval 2.7-11.9) for a CRP level in the upper quartile. Multivariate analysis demonstrated the independence of the relation between CRP levels and in-hospital mortality (p = 0.0001). No significant differences in CRP level were found among deceased patients classified by cause of death (heart rupture 44%, pump failure 41%, comorbidity 5%). CONCLUSIONS: CRP concentration is raised in many old patients with acute myocardial infarction and seems to independently stratify patients for in-hospital mortality risk. This prognostic information may assist in providing the appropriate level and duration of close monitoring and be an additional support to evaluate the risk-benefit ratio of thrombolytic therapy in some cases.

Aged↗
PubMed1998

Aortic intramural hematoma: an increasingly recognized aortic disease.

Aortic intramural hematoma (IMH) is a rarely diagnosed pathological condition that is not well characterized to date. We diagnosed IMH in 4 of 31 patients with suspected aortic dissection admitted to our coronary care unit from 1992 to 1995. In all 4 cases, IMH was located in the ascending aorta. At the time of hospitalization, all patients showed tachycardia, hypotension and pericardial effusion. Diagnosis of IMH was made by transesophageal echocardiography and computed tomography. We performed aortography in 2 patients, but it was non-diagnostic in both of them. One patient died before surgery. Autopsy confirmed the diagnosis of IMH and showed severe pericardial effusion. In another patient, the diagnosis was confirmed during successful surgery, while the remaining 2 patients recovered after medical therapy. The 3 surviving patients are still under follow-up control 12, 16 and 20 months after the initial acute event. We briefly discuss the epidemiological, clinical, diagnostic, therapeutic and prognostic aspects of IMH.

Aged↗
PubMed1996

Threshold energy dose for enzyme release after direct-current countershock.

Serial measurement of serum total creatine kinase and creatine kinase MB isoenzyme was prospectively performed by photometric assay in 82 consecutive patients (55 male and 27 female; mean age 62 +/- 11 years) after elective DC countershock for atrial flutter or fibrillation. Enzyme release is commonly observed to follow DC shock; the related energy threshold for enzyme release, however, a parameter with potential clinical usefulness, has not yet been determined. The energy dose was individually titrated but the anterolateral paddle-electrode location was used in all cases. The mean +/- S.D. (range) of shock number, peak energy level and cumulative energy dose normalized to body weight were respectively: 1.7 +/- 0.9 (1-5), 228.6 +/- 87.6 (75-400) J and 5.26 +/- 3.74 (1.0-19.7) J/kg. All these parameters had highly significant positive correlation with enzyme release (P < 0.0001), which peaked 16 h after countershock. Only creatine kinase levels changed significantly vs. baseline (P < 0.0001). As evidenced by dose vs. effect scattergram, the energy threshold value for enzyme release was around 4 J/kg for creatine kinase and 6 J/kg for creatine kinase MB isoenzyme. These energy dose figures may provide clinical usefulness to avoid unnecessary muscle damage; moreover, they may be used as a reference when enzyme elevations interfere with the diagnosis of a concomitant ischemic acute myocardial infarction.

Adult↗
PubMed1995

[Recent morphofunctional findings on the left atrium: their relations to thromboembolic risk].

In the past, the left atrial appendage has been considered a "useless" structure but associated to thromboembolic complications; its physiologic role is still undefined. Owing to its great distensibility, left atrial appendage positively influences atrial compliance and left ventricular performances. In addition this structure seems to play an important role in circulatory homeostasis by the release of atrial natriuretic factor in response to volume loading and atrial stretch. Transesophageal echocardiography provides a detailed anatomical characterization of this structure and, by means of Doppler flow velocities recordings, supplies relevant functional data. Despite their anatomical contiguity, the left atrium and atrial appendage result from a separate embryonic development; likewise, their function may differentiate. In the left atrial appendage a quadriphasic flow pattern has been described in subjects with sinus rhythm; however, as we reported, in some patients a more complex Doppler pattern can be observed, with an additional systolic forward flow wave which is presumably due to reflection phenomena. In patients with atrial fibrillation, an irregular flow pattern has been detected, which is mostly dependent on the duration of the arrhythmia, the underlying heart disease and the left atrial pressure. By transesophageal echocardiography a clear correlation has been established between the left atrial appendage slow flow and the occurrence of thromboembolic events; however, while waiting data from large studies, stratification of patients according to thromboembolic risk and decisions about anticoagulant prophylaxis should be performed by clinical information and transthoracic echocardiographic findings. No clinical or echocardiographic parameter has been found to be predictive of the thromboembolic events after cardioversion; in this setting the exclusion of atrial or atrial appendage thrombi by transesophageal echocardiography does not rule out the need for anticoagulation in patients with atrial fibrillation undergoing electrical or pharmacological cardioversion.

Atrial Function, Left↗
PubMed1994

Do inotropic drugs always induce a positive lusitropic effect? A comparison between k-strophanthidin and dobutamine in patients with coronary artery disease.

The interaction between systolic and diastolic effects of inotropic drugs is an important subject which has not yet been fully clarified in the cardiological literature. The effects of the inotropic drugs k-strophanthidin and dobutamine on left ventricular (LV) relaxation and early filling phase were compared in patients with coronary artery disease (CAD) and preserved systolic function. Twenty-two patients were randomly divided into two groups; group I was infused with 0.0035 mg.kg-1 of k-strophanthidin for 10 min and group II with dobutamine at a rate of 10 micrograms.kg-1.min-1 for 10 min. Both groups underwent simultaneous haemodynamic and echo 2D-Doppler evaluations at controlled heart rate. K-strophanthidin improved contractility indexes (peak of LV systolic pressure P < 0.001, max dP/dt + P < 0.05 and dP/dt P < 0.01) and worsened T constant and LV lowest diastolic pressure, (LVLDP) (P < 0.001 and P < 0.05 respectively) without changing early transmitral filling parameters. Dobutamine induced a significant increase in contractility in group II but at the same time significantly improved LV relaxation variables (max dP/dt - P < 0.01 and T constant P < 0.001). In addition, dobutamine reduced LVLDP (P < 0.05) and significantly increased LV early filling parameters. These results show that an acute administration of either k-strophanthidin or dobutamine enhances contractility, whereas these drugs have the opposite effect on the early diastolic phase.

Age Factors↗
PubMed1993

Effect of dobutamine on left ventricular relaxation and filling phase in patients with ischemic heart disease and preserved systolic function.

The beneficial effects of dobutamine on left ventricular systolic and diastolic phases have been described in patients with congestive heart failure. Its influence on left ventricular diastolic phase in patients with preserved systolic function, absence of dys- or akinetic areas, and left ventricular dilatation has not yet been adequately investigated. Thus a simultaneous echo-Doppler and hemodynamic study was performed in 15 patients with ischemic heart disease and preserved systolic function in order to assess the effect of dobutamine on left ventricular relaxation and filling phase. The infusion of dobutamine at a rate of 10 micrograms/kg/min induced a marked inotropic action, as shown by the significant increase in positive dP/dt (from 1392 +/- 224 to 2192 +/- 295 mmHg/sec, p < 0.001), dP/dt/P (from 32 +/- 8.1 to 50 +/- 17 sec-1; p < 0.0001), and in peak of systolic pressure (from 143 +/- 25 to 168 +/- 36 mmHg; p < 0.005). In addition, dobutamine reduced the end-systolic volume index (from 30 +/- 16 to 26 +/- 19 ml/m2; p < 0.05), the end-systolic stress (from 222.2 +/- 65.3 to 198.4 +/- 84 g/cm2; p < 0.006), and had favorable effects on relaxation and the early filling phase.(ABSTRACT TRUNCATED AT 250 WORDS)

Dobutamine↗
PubMed1992

Effects of acute K-strophantidin administration on left ventricular relaxation and filling phase in coronary artery disease.

In 10 patients with coronary artery disease, preserved left ventricular (LV) performance and absence of previous myocardial infarction, the effects of an acute intravenous administration of k-strophantidin (0.005 mg/kg over 10 minutes) on selected parameters of both LV systolic and diastolic function, including relaxation, were evaluated. An increase in positive first derivative of LV pressure (dP/dt) and in the ratio between dP/dt and the pressure developed (dP/dt/P) (1,530 +/- 287) 1,600 +/- 329 mm Hg/s [p less than 0.05], and 30 +/- 6 to 34 +/- 8 s-1 [p less than 0.05], respectively) demonstrated the inotropic effect of k-strophantidin, whereas volumetric parameters of systolic function (end-systolic and stroke volume indexes, and ejection fraction) did not show any significant change. However, LV relaxation was impaired by k-strophantidin injection; in fact, mean values of T constant were significantly increased from 50 +/- 12 to 55 +/- 13 ms (p less than 0.01). Lowest LV and end-diastolic pressures increased from 8 +/- 4 to 11 +/- 4 mm Hg (p less than 0.05) and from 17 +/- 6 to 20 +/- 8 mm Hg (p less than 0.05), respectively. The end-diastolic volume and maximal rate of volumetric increase during the early and late filling phases were not modified by k-strophantidin. Mean aortic pressure increased from 110 +/- 10 to 120 +/- 12 mm Hg (p less than 0.001). Therefore, in patients with coronary artery disease and LV preserved performance, an acute intravenous administration of k-strophantidin appears to stimulate contractility and to worsen relaxation, and minimal LV and end-diastolic pressures.

Aged↗
PubMed1991

Peak aortic blood acceleration: a possible indicator of initial left ventricular impairment in patients with coronary artery disease.

In 25 patients undergoing diagnostic cardiac catheterization, a catheter-tip electromagnetic velocity transducer was used to evaluate maximum velocity and acceleration of blood in the ascending aorta. All patients underwent a complete haemodynamic evaluation, including high-fidelity recording of intraventricular pressures and calculation of the derived indices, left ventriculography and coronary angiography. Nineteen patients with critical coronary stenoses were divided according to the presence of signs of left ventricular dysfunction, while the control group consisted of six subjects with chest pain, but without cardiac abnormalities detectable by cardiac catheterization. Maximum aortic acceleration was significantly lower in coronary patients (378 +/- 130 vs 562 +/- 82 in the control group P less than 0.01) and also in the selected subgroup of coronary patients with normal haemodynamic and angiographic indices of left ventricular systolic function (310 +/- 102 vs 562 +/- 82, P less than 0.01). No relationship could be observed between maximal blood acceleration and left ventricular peak systolic pressure, +dP/dt, left ventricular end-systolic volume index and ejection fraction. Our results suggest that maximal blood acceleration from the left ventricle may detect an initial myocardial impairment in patients with definite coronary artery disease but with normal conventional indices of left ventricular function. The clinical interest of this index, however, is limited by overlapping values in patients with and without coronary artery disease and the inability of a further separation of ischaemic patients in accordance with the severity of left ventricular impairment and the extension of coronary artery involvement.

Adult↗
PubMed1988

[Chronic treatment of dilated cardiomyopathy by beta blocking agents. Clinical and hemodynamic follow-up].

symptomatic dilated cardiomyopathy were studied in order to evaluate the effect of long term sympathetic beta-blockade with metoprolol. Clinical evaluation, stress test, two-dimensional echocardiography, 24 hour ambulatory electrocardiography and hemodynamic assessment with Swan-Ganz catheter were performed before enrollment in the study. Patients were randomly assigned to the relative placebo (8 pts) or metoprolol group (12 pts) in a single-blind fashion. The placebo group received standard therapy (digitalis, diuretics, vasodilators and anticoagulants as needed), while the metoprolol group, along with standard therapy received low-dose beta-blockade, starting with 6.25 mg twice daily and then doubling every 4 days on the two daily administrations. The therapeutic end-point was 100 mg. Patients received less than 100 mg if their systolic blood pressure was less than 100 mmHg or if their resting heart rate was less than 55 beats/min. Patients were clinically assessed every month and a 24-hour electrocardiography, echocardiography and hemodynamic control was repeated after six months. In the metoprolol group there was one sudden death and two drop-outs.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1986

[Effect of propafenone on the pharmacokinetics of digoxin administered orally: a study in healthy volunteers].

It is well known that many cardiovascular drugs affect digoxin kinetics, but nothing is defined on propafenone-digoxin interaction. To clarify this problem, we studied digoxin kinetics in 8 healthy men, who received digoxin oral dose (0.50 mg) in the control state and again during maintenance therapy with propafenone (150 mg q.i.d.). Statistically significant changes were observed during propafenone in a number of digoxin kinetic indexes: a rise in peak serum digoxin concentration (4.30 vs 3.07 ng/ml - p less than 0.005), in area under the serum-digoxin concentration curve (4 h: 520.4 vs 368.9; 10 h: 789.6 vs 621.3 ng X min/ml - p less than 0.005; 24 h: 1187.6 vs 954.7 ng X min/ml - p less than 0.05) and urinary excretion of digoxin (277.7 vs 203.5 mcg - p less than 0.005). Renal digoxin clearance was not affected by propafenone. We conclude that propafenone interact kinetically with digoxin in healthy subjects, perhaps increasing digoxin bioavailability.

Administration, Oral↗