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S Dalla-Volta

Publications and source records attributed to S Dalla-Volta.

At least 19 recordsLinked to original sources
PubMed1999

Analytical expression of effective afterload in aortic and mitral regurgitation.

Effective arterial elastance (Ea) is the coupling parameter between the left ventricle and peripheral circulation in normal subjects. If left ventricular end systolic pressure (Pes), contractility (Es) and Ea are known, left ventricular end diastolic volume (LVEDV) and ejection fraction of the ventricle are completely determined. The aim of this study was to give an analytical expression for Ea in patients with mitral and aortic regurgitation, and predict both LVEDV and the effect of vasodilator therapy on LVEDV. Twenty-three subjects with atypical chest pain, 15 patients with mitral insufficiency and 11 with aortic insufficiency underwent diagnostic cardiac catheterization, coronary angiography, and left ventricular cineangiography, which was analyzed quantitatively. Ea was 2.05 +/- 0.63 in normal subjects, while it was 1.28 +/- 0.71 and 1.57 +/- 0.87 in patients with mitral and aortic insufficiency, respectively. All these groups differed with ANOVA test (p = 0.0031). We tested the ability of the analytical expressions for Ea in normal subjects, and patients with mitral insufficiency or aortic insufficiency to predict measured Ea and LVEDV. Ea and LVEDV were predicted rather accurately in every case (p < 0.0001). We used published data to test the effect of resistance modulation on LVEDV. Predicted and measured LVEDV were linearly correlated both in aortic (p < 0.0001) and mitral insufficiency (p = 0.027). Moreover, in some cases a left ventricular enlargement after vasodilator therapy could be anticipated because of an unbalanced decrease in resistance and heart rate. Ea seems to be the coupling parameter between the left ventricle and the peripheral circulation not only in normal subjects, but also in patients with mitral or aortic regurgitation; its measurement before administering vasodilating drugs may be useful in order to predict the effects on LVEDV, and achieve an optimal ventriculoarterial coupling.

Aortic Valve Insufficiency↗
PubMed1999

Transaortic gradient is pressure-dependent in a pulsatile model of the circulation.

BACKGROUND AND AIM OF THE STUDY: Although the transvalvular gradient is described as flow-dependent, pressure-dependence of the gradient, irrespective of flow, has not been demonstrated. METHODS: The Sheffield pulse duplicator equipped with a X-Cell 21 porcine valve mounted in the aortic position was used. Transaortic gradient was measured at a constant rate of 80 beats/min, while flow was kept at 2, 5 or 8 l/min, and systemic pressure was increased up to 200 mmHg by adjusting peripheral resistance manually. Valve area was computed with the Gorlin formula. A total of 87 measurements was carried out. RESULTS: For each flow, transvalvular gradient increased linearly with pressure, and computed area decreased. The slope of the pressure-gradient relationship was independent of flow. CONCLUSION: Transaortic gradient depends not only on flow, but also shows pressure-dependency that should be taken into account when evaluating aortic stenosis, especially in hypertensive and hypotensive states.

Aortic Valve↗
PubMed1997

Troponin T, creatine kinase MB mass, and creatine kinase MB isoform ratio in the detection of myocardial damage during non-surgical coronary revascularization.

The presence of myocardial injury during non-surgical coronary revascularization has been evaluated by means of highly specific and sensitive biochemical markers. Troponin T, creatine kinase-MB isoenzyme mass concentration, and creatine kinase MB2/MB1 isoform ratio have been determined in 80 patients who underwent coronary revascularization with percutaneous transluminal coronary angioplasty (PTCA). Forty-five patients underwent balloon angioplasty, 15 rotational atherectomy, 10 directional atherectomy, and 10 elective coronary stenting. Serum concentration of the evaluated markers did not increase significantly after 57 uncomplicated revascularization procedures, including 15 rotablation procedures, nor after 8 PTCAs complicated by localized coronary type B and C dissections. Significant elevation of all markers above the upper limits of the reference interval (P < 0.05) was detected after occlusion of small side branches (< 0.5 mm diameter) in 5 patients. Creatine kinase MB2/MB1 isoform ratio was the earliest marker to increase. After recanalization of occluded vessels in 8/10 patients with 6-60 days old myocardial infarction only troponin T concentrations increased from a baseline of 0.28 microgram/l to a median peak of 0.80 microgram/l. This increase was statistically not significant (P = 0.12). In conclusion, myocardial damage was not detected following uncomplicated non-surgical revascularization obtained with different techniques. Markers of myocardial injury provide high sensitivity after small side branch occlusion.

Aged↗
PubMed1995

Safety and efficacy study of delapril versus enalapril in patients with congestive heart failure.

The results after the first 6 months of the 1-year treatment of this multicenter, randomized, open, parallel-group design study of delapril versus enalapril in patients with congestive heart failure (CHF), New York Heart Association (NYHA) classes II and III, are presented. The initial dose of delapril (7.5 mg twice daily) and enalapril (2.5 mg twice daily) could be doubled on a 2-weekly basis (from the beginning of the study) to a maximum of 30 mg twice daily and 10 mg twice daily, respectively. The evaluation of the efficacy was based on the changes of NYHA class, results of exercise testing involving bicycle ergometry (duration of exercise, workload, work performed, double product) performed before and after 3 months' treatment, echocardiography (left ventricular end-diastolic volume and end-systolic volume, ejection fraction, and left ventricular wall stress) at baseline and after 3 and 6 months of treatment and changes in cardiothoracic ratio, electrocardiography, and NYHA class, and patient's opinion of efficacy. Safety was evaluated by monitoring the adverse reactions, laboratory tests, and blood pressure. At 3 months, both treatments had produced a significant improvement compared with baseline in the duration of exercise, workload, and work performed in the bicycle ergometry test as well as in the ejection fraction and in left ventricular wall stress after 6 months of treatment. In addition, after 3 and 6 months of treatment, delapril produced a significant decrease in left ventricular end-systolic volume. Improvement of at least one NYHA class was observed in 20% of delapril patients and 14% of enalapril patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Myocardial dysfunction and abnormal left ventricular exercise response in autonomic diabetic patients.

In diabetic patients, the pathophysiologic mechanisms of exercise-induced left ventricular (LV) dysfunction remain controversial. In this study, the role of myocardial contractility recruitment in determining an abnormal LV response to isometric or dynamic exercise has been investigated in 14 diabetic patients with autonomic dysfunction. Ischemic heart disease was excluded by the absence of LV wall motion abnormalities induced by isotonic and isometric exercise and by coronary angiography. Left ventricular and myocardial function were studied at rest, and during isometric and isotonic exercise, by two-dimensional echocardiography; moreover, recruitment of an inotropic reserve was assessed by postextrasystolic potentiation at rest and at peak handgrip. An abnormal response of LV ejection fraction to isometric (9/14) or to dynamic (8/14) exercise was frequent in study patients. In these patients, baseline myocardial contractility was normal, and the significant increase in ejection fraction by postextrasystolic potentiation indicated a normal contractile reserve (65 +/- 7% vs. 74 +/- 6%, p = 0.001). Nevertheless, the downward displacement of LV ejection fraction-systolic wall stress relationships during exercise suggests an inadequate increase in myocardial contractility. However, the abnormal ejection fraction at peak handgrip was completely reversed by postextrasystolic potentiation (67 +/- 6% vs. 58.1 +/- 10%, p = 0.008), a potent inotropic stimulation independent of the integrity of adrenergic cardiac receptors. A defective inotropic recruitment, despite the presence of a normal LV contractile reserve, plays an important role in deexercise LV dysfunction in diabetic patients with autonomic neuropathy.

Adult↗
PubMed1995

Simulation of chronic mitral regurgitation.

In mitral regurgitation the left ventricle enlarges in order to increase its stroke volume because of the regurgitation through the mitral valve. The amount of this volume increase, and of the consequent increase in left ventricular mass, its dependent upon the amount of the regurgitant volume, but many other factors come into play, such as left ventricular pumping capability (contractility), the level of peripheral pressure, resistance and compliance of the arterial tree. The aim of this study is to predict the final left ventricular volumes and mass given the amount of mitral regurgitation. The predicted results are compared with actual data in real patients. In most cases prediction is fairly good; some discrepancies can be interpreted as an index of advanced decompensation.

Cardiac Output↗
PubMed1994

Reversible contractile dysfunction of viable myocardium. Implications for decision making process in post-infarction patients.

Myocardial dysfunction and silent myocardial ischemia have been identified as important prognostic factors following acute myocardial infarction, also in low risk patients. In postinfarction patients, impaired left ventricular function is the result of fixed scar and reversible contractile dysfunction of viable stunning or hibernating myocardium. Post-extrasystolic potentiation (PESP) during 2-dimensional echocardiographic monitoring may be used to detect the presence of viable myocardium in asynergic myocardial segments. Incidence of reversible contractile dysfunction is a very common phenomenon at predischarge examination after myocardial infarction in asymptomatic patients, and it is independent on the persistence of silent ischemia. A progressive loss of myocardial viability occurs over the first year following the acute phase despite the maintenance of an asymptomatic clinical status. This phenomenon is associated with significant dilatation of the left ventricle. Moreover, silent ischemia is strongly related with this progressive loss of myocardial viability and left ventricular dilatation. Thus, it becomes evident that the most important role of medical and interventional approaches consists of limiting the acute necrosis by reperfusion and in preventing the loss of viable chronically hypoperfused myocardium that appears to be a major factor of left ventricular remodeling and changes over time of prognostication in individual patients. Finally, the presence of viable myocardium by PESP in the arterial zone at risk is highly predictive of 4-year mortality, particularly in patients with low ejection fraction (< 40%), and identifies patients who are suitable candidates for revascularization after myocardial infarction.

Echocardiography↗
PubMed1993

Silent ischemia and loss of reversible myocardial dysfunction following myocardial infarction.

Sixty-seven asymptomatic patients were enrolled after a first uncomplicated myocardial infarction (MI) so as to study the relevance of reversible myocardial dysfunction in determining left ventricular function soon after the acute episodes and 12 months later. Moreover, the potential role of silent ischemia in conditioning the evolutive aspects of contractile dysfunction has been investigated. Postextrasystolic potentiation during two-dimensional echocardiographic (2-D echo) monitoring has been used to detect the presence of viable myocardium in asynergic myocardial segments. Results of electrocardiographic (ECG) ambulatory monitoring at predischarge determined patient groups: Group A included 49 patients without ST changes during monitoring, while Group B included 18 patients with silent ischemia. Incidence of reversible myocardial dysfunction was similar in the two study groups (82 vs. 86%, p = NS). Group B patients were older (59.6 +/- 6.7 vs. 50.6 +/- 10.6 years, p < 0.015) and had lower ejection fractions (EFs, 43.4 +/- 6.4% vs. 51.2 +/- 8.3%, p = 0.026) and higher at-rest wall-motion scores (WMSs, 11.4 +/- 5.9 vs. 7.2 +/- 3.8, p = 0.019). Left ventricular end-diastolic volume (LVEDV) and potentiated WMS did not differ. At 1-year examination, Group B patients exhibited a greater LVEDV index (96 +/- 6.5 vs. 70.7 +/- 14 ml/m2, p < 0.002) with a worsening both in rest and in potentiated wall-motion score index (12.8 +/- 4.6 vs. 5.3 +/- 1.8, p < 0.001; 9.2 +/- 3.6 vs. 4.8 +/- 2.2, p < 0.001, respectively). Left ventricular EF remained significantly depressed in Group B patients (42 +/- 8.7% vs. 55.5 +/- 8.1%, p < 0.002).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

PAIMS 2: alteplase combined with heparin versus heparin in the treatment of acute pulmonary embolism. Plasminogen activator Italian multicenter study 2.

BACKGROUND: The effect of alteplase versus heparin in pulmonary embolism has not been studied extensively with serial pulmonary angiograms. OBJECTIVES: The aim of this randomized, open trial was to evaluate the efficacy and safety of alteplase followed by heparin, versus heparin alone, in 36 patients with angiographically documented pulmonary embolism. METHODS: Twenty patients were allocated randomly to a 2-h infusion of alteplase (10 mg bolus, then 90 mg over 2 h) followed by heparin; the other 16 patients were given intravenous heparin at a continuous infusion rate of 1,750 IU/h. RESULTS: The vascular obstruction, assessed by the Miller index at pulmonary angiography, decreased significantly in alteplase-treated patients (p less than 0.01) from a baseline of 28.3 +/- 2.9 to a value of 24.8 +/- 5.2 2 h after the start of infusion; in the heparin group there was no change (from 25.3 +/- 5.3 to 25.2 +/- 5.4). Mean pulmonary artery pressure decreased significantly from a baseline of 30.2 +/- 7.8 mm Hg to 21.4 +/- 6.7 in the alteplase group and increased in the heparin group (from 22.3 +/- 10.5 to 24.8 +/- 11.2 mm Hg). For a subset of patients, lung scans were performed at baseline and on days 7 and 30. There were no differences between the two groups in the follow-up lung scans, but there were significant decreases from the baseline values. Bleeding occurred in 14 of 20 alteplase-treated patients and in 6 of 16 in the heparin group (p = NS). There were three major bleeding episodes in the alteplase group and two in the heparin group. Two patients died after fibrinolysis (one of acute renal failure after cardiac tamponade and one of cardiac arrest after cerebral hemorrhage) and one patient in the heparin group died of recurrent pulmonary embolism. CONCLUSIONS: Alteplase resulted in a greater and faster improvement of the angiographic and hemodynamic variables compared with heparin. However, the high frequency of bleeding observed with alteplase in this trial suggests that patients should be carefully selected before thrombolytic therapy is given.

Acute Disease↗
PubMed1992

Reversible and irreversible left ventricular dysfunction after acute myocardial infarction.

Left ventricular function after acute myocardial infarction depends on several mechanisms leading to left ventricular remodeling: (a) infarct size and healing and (b) adaptive changes involving both the dysfunctioning but viable myocardium (hibernating and stunned myocardium) and the nonischemic myocardium. The prognosis after acute myocardial infarction is strongly related to regional and global left ventricular function and the loss of dysfunctioning viable myocardium is a main factor in the worsening in left ventricular function in survivors of the acute phase. Thus, medical strategies should exert their beneficial effect on the "mechanical instability" of ventricular myocardium by saving the viable myocardium. beta-Blocker therapy has been shown to be effective in improving the prognosis via anti-ischemic and antiarrhythmic actions. The combination of metoprolol and nisoldipine seems to be able to preserve the contractile function of viable myocardium in the first 6 months after acute myocardial infarction.

Adrenergic beta-Antagonists↗
PubMed1991

Exercise-induced left ventricular dysfunction in coronary heart disease. A model for studying the stunned myocardium in man.

The concept of myocardial stunning encompasses a wide variety of settings with major pathophysiological differences. Stresses, such as exercise-provoked myocardial ischaemia and dysfunction, are accompanied in most patients by a flow-limiting coronary stenosis, while contractile dysfunction persists in some with cessation of exercise. Twenty-six patients with proven coronary artery disease were studied by exercise echocardiography. Left ventricular (LV) volumes, wall motion and myocardial thickening were detected in apical four- and two-chamber views at rest and during upright bicycle exercise. All patients had an increase in total asynergy score and a decrease in ejection fraction (EF) during exercise. Myocardial dysfunction persisted after exercise in 22 patients (84%) as shown by the persistence of low values of LVEF on recovery up to 30 min. When compared to control, nisoldipine reduces total asynergy score and prevents the decline in LVEF during exercise by reducing the extent of myocardial ischaemia. The value of LVEF on recovery is normal. Thus, this particular form of myocardial stunning after exercise-induced ischaemia offers an interesting model for studying (1) the susceptibility of an individual patient and (2) to test the capability of a drug to prevent and to reverse myocardial stunning.

Adult↗
PubMed1990

Comparison of trimetazidine with nifedipine in effort angina: a double-blind, crossover study.

Trimetazidine has been shown to have an antianginal effect, increasing exercise capability without producing any significant change of heart rate or systolic blood pressure. The aim of this study was to compare trimetazidine efficiency to that of another classical antianginal drug. A double-blind crossover trimetazidine versus nifedipine trial was carried out in 39 male patients, mean age 58 years, with effort angina for 5 years on average, and a mean number of weekly attacks of 2.4. Thirteen patients had previous myocardial infarction. Nineteen patients received nifedipine (40 mg per day) then trimetazidine (60 mg per day), and 20 patients received the drugs in the opposite order. Each therapeutic period of 6 weeks was preceded by 1 week of washout with placebo. Drug efficacy was assessed by a bicycle exercise tolerance test, performed at the beginning and at the end of each therapeutic period, and by clinical symptoms observed with placebo or with treatment. The statistical analysis was performed according to a crossover design, with repeated measurements. The decrease of the number of weekly attacks was not significantly different with trimetazidine and nifedipine. Results on the exercise test showed no significant differences for maximum workload, the duration of exercise, ST-segment depression at peak exercise, and the time to 1-mm ST-segment depression. Heart rate and systolic blood pressure were not significantly different at rest and at peak exercise. However, the change in the rate-pressure product at the same workload differed significantly between the drugs: It decreased with nifedipine and remained unchanged with trimetazidine, indicating the difference to be in the mode of action of the drug.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Long-term nifedipine unloading therapy in asymptomatic patients with chronic severe aortic regurgitation.

Vasodilating agents acutely reduce regurgitant volume and improve left ventricular performance in aortic regurgitation, but more information is necessary about their long-term efficacy. To evaluate the effects of 12 months of therapy with nifedipine, a randomized, double-blind, placebo-controlled trial was performed in 72 asymptomatic patients with severe aortic regurgitation. At 12 months, patients receiving nifedipine had a significant reduction in left ventricular end-diastolic volume index (110 +/- 19 versus 136 +/- 22 ml/m2, p less than 0.01) and mass (115 +/- 19 versus 142 +/- 16 g/m2, p less than 0.01) measured by two-dimensional echocardiography. They also had a reduction in left ventricular mean wall stress (360 +/- 27 versus 479 +/- 36 kdyne/cm2, p less than 0.001) and an increase in ejection fraction (72 +/- 8% versus 60 +/- 6%, p less than 0.05). These data show that the long-term unloading action of nifedipine is able to reverse left ventricular dilation and hypertrophy and suggest that such therapy has the potential to delay the need for valve replacement in asymptomatic patients.

Adult↗
PubMed1990

The concept of preload and its evaluation in the intact left ventricle.

Preload affects left ventricular pump function through the Frank-Starling curve by changing sarcomere length. However, common indices of preload, such as end-diastolic volume, or pressure, or stress, do not necessarily reflect sarcomere length. Ultimately, this depends on the elastic stiffness constant (k) and end-diastolic stress (sigma), which are not in simple relation with the above mentioned indices. An index of preload is proposed, (k sigma)(1/k). This index has been evaluated in 148 patients with different degrees of hemodynamic overload, and in 24 normal subjects. The preload index was found to be 1.448 +/- 0.034 in normal subjects. However, in the other patients evaluated preload index increased in mitral insufficiency (1.490 +/- 0.035), in decompensated aortic insufficiency (1.490 +/- 0.89) and in dilated cardiomyopathy (1.52 +/- 0.125), and markedly decreased in aortic stenosis (1.367 +/- 0.039) and in hypertrophic cardiomyopathy (1.41 +/- 0.034). It was always positively related to the afterload, measured as peak systolic stress. No positive relationship was found with end-diastolic volume nor pressure. Therefore, preload as a compensatory mechanism is differently recruited in response to various degrees of hemodynamic overload and parallels the afterload, in agreement with the concept of preload-afterload mismatch.

Aortic Valve Insufficiency↗
PubMed1989

Contribution of cross-sectional echocardiography to the diagnosis of right ventricular dysplasia at the asymptomatic stage.

The value of cross-sectional echocardiography in the early diagnosis of right ventricular (RV) dysplasia in asymptomatic patients has been assessed. Criteria that defined RV dysfunction and structural abnormalities were developed from 38 normal subjects. Of 136 patients admitted into the study program, 40 (29.4%) had an echocardiogram suggestive of RV dysplasia using the following criteria: mild dilatation of the right ventricle (normal range defined as the 95% confidence limit of the values in the control group); localized bulge and dyskinesia of the infero-basal wall; structural changes of the moderator band; isolated enlargement of RV outflow tract; apical dyskinesia and trabecular disarrangement. Holter monitoring and a maximal exercise stress test at entry into the study and during the follow-up (mean 42, range 18-82 months) demonstrated serious ventricular arrhythmias, and RV endomyocardial biopsy confirmed the diagnosis of RV dysplasia in most of these patients, characterized by an electrical instability of RV myocardium (82.5%). During the follow-up, a marked enlargement of RV cavity appeared in three other patients, and RV endomyocardial biopsy demonstrated the typical findings in all patients.

Adolescent↗
PubMed1988

Myocardial function in heart failure.

Overt cardiac failure usually presents with constant clinical features as consequences of the reduced pump action, associated with an increased adrenergic drive, independent of the underlying disease. However, the study of left ventricular function, before and during the phase of cardiac insufficiency, shows that different pathophysiological mechanisms are responsible for the symptoms and signs of reduced cardiac action. It is possible to recognize that cardiac failure is caused primarily by: (1) early severe depression of the inotropic state, i.e. dilated cardiomyopathies; (2) late inadequate level of ventricular hypertrophy, with normal contractility, i.e. aortic stenosis; (3) early inadequate level of hypertrophy and slightly reduced inotropic state, i.e. mitral insufficiency, and (4) late inadequate level of hypertrophy and severe progressive reduction in contractility, i.e. aortic insufficiency. The possibility of an 'in vivo' assessment of the different determinant parameters of left ventricular function (contractility, afterload, preload, fiber and chamber compliance) through echocardiography enables a better understanding of the mechanisms leading to the cardiac failure and a more efficient therapeutic approach.

Echocardiography, Doppler↗
PubMed1988

Observations on the capability of the electrocardiogram to detect left ventricular function in chronic severe aortic regurgitation.

Echocardiographic parameters of left ventricular (LV) function were compared with the electrocardiographic findings in 40 patients with chronic severe aortic regurgitation. Total 12-lead QRS amplitude was linearly correlated with LV mass and its 'relative reduction' (less than 250 mm) indicated LV hypertrophy. Patients with an electrocardiographic 'strain' pattern had a marked increase LV stress (573 +/- 68 dyn). The association of high total 12-lead QRS amplitude and 'strain' indicate a moderately depressed ejection fraction (EF = 43 +/- 3). Finally, 'strain' and a 'relative reduction' of total 12-lead QRS amplitude were present in patients with a severe depression of EF and contractility. The predictive value of these electrocardiographic indices was confirmed during a mean follow-up of 49 months. In conclusion, the electrocardiogram remains an excellent, easy tool for anatomical and functional investigation of patients with aortic regurgitation.

Adolescent↗