Captopril versus frusemide in moderate heart failure.
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Biomedical subjects
Publications and source records attributed to A Boccanelli.
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A multicenter double-blind placebo-controlled investigation was carried out in 42 patients with severe congestive heart failure who were given ibopamine (SB-7505), the 3,4-diisobutyryl ester of N-methyldopamine, for a period of 10 days in addition to previous treatment with digitalis and diuretics. Symptoms were evaluated by using a suitable score; some patients were submitted to an exercise test along with other clinical tests. Compared with placebo, ibopamine induced no significant changes in heart rate and arterial blood pressure. Clinical scores were lower after ibopamine than after placebo (p less than 0.01). Functional capacity, defined as the duration (in s) of a maximum symptom-limited exercise test using the ergometric bicycle with a constant 25-W workload, was significantly higher after ibopamine than after placebo (p less than 0.05). So a clear symptomatic improvement was observed after ibopamine in cardiac patients with prolongation of exercise time and reduced clinical scores. In conclusion, the results obtained, along with the slight improvement in the systolic time intervals, indicate that ibopamine is capable of improving cardiac performance in patients with advanced heart failure who display symptoms despite treatment with digitalis and diuretics.
In 15 patients with moderate congestive heart failure not completely controlled on digoxin (0.25 mg o.d.) and frusemide (25 mg o.d.), we compared the addition of captopril (12.5 to 50 mg b.i.d.) with increasing doses of frusemide (25 to 100 mg o.d.), in a randomized double-blind, double-dummy, comparative trial. Thirteen patients completed the 3 months study: two dropped-out in the frusemide group. Statistically significant clinical improvement occurred in both treatment groups. Exercise tolerance also significantly improved in both groups in a parallel fashion. Echocardiographic cardiac function data showed a significantly better pattern of changes in the captopril group. The addition of low doses of captopril to basal therapy seems to be as effective as the addition of high doses of frusemide in uncontrolled moderate congestive heart failure. This approach with captopril also appears to be more physiological and safe.
During Ergonovine-test a patient with Prinzmetal angina presented (in I, aVL, V3-V6) ST downsloping which, after a temporary phase of alternative normalization (AST) beat to beat in V5, progressed to ST upsloping with typical angina. The M-mode echo-study first discovered, before than ecg, septal impairment (hypokinesia which increased to akinesia in the AST phase) and also asynergy of posterior wall of left ventricle. After intravenous nitrate echo-alterations reversed more rapidly than ecg one (transitional phase of ST decrease). The authors relate the AST to temporary alternative pseudonormalization caused by a phase of electrical instability during progressive vasospastic ischemia involving first the endocardial layers and after the epicardium of a single myocardiocoronary district. Probably also other partially opposite ischaemic districts, as suggested from echo data of posterior wall asynergy took a part in these events. This rare ST-alternans type as new pseudonormalization phenomenon and the usefulness of echo-study during ischaemic attacks are stressed.
The value of pulsed Doppler echocardiography in assessing the presence and severity of tricuspid regurgitation (TR) has been studied in three groups of subjects, 12 without cardiovascular disease (Group I), 38 with TR (Group II) and 16 patients with aortic and mitral valve disease but no TR (Group III). The presence and severity of TR was also independently evaluated by clinical examination, jugular vein pulse recording and/or hemodynamic investigation. Left parasternal, sub-xyphoid and apical views were adapted for the pulsed Doppler echocardiographic examination. The sample volume was placed in the right atrium at varying distances from the tricuspid valve. We tried to quantitate the degree of TR according to: 1) the diameter and maximal distance from the tricuspid valve of the regurgitant stream, 2) the duration of reguritation through systole, and 3) the degree of turbolence as demonstrated by the time interval histograms. On the basis of above mentioned criteria, three subgroups of subjects with TR, i.e. mild, moderate and severe were recognised. These results were compared to hemodynamic and/or clinical-poligraphic evaluation. In 34 Group II subjects (89%), the Doppler study revealed the presence of TR and allowed an acceptable quantitative assessment. Falsely positive diagnoses were not made in any of the subjects of Group I. Identification of organic TR in patients with atrial fibrillation was possible only when regurgitation was moderate or severe.
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A new echocardiographic technique is presented: echocardiokymography. Parietal and valvular motion patterns are condensed in a single, two-dimensional image, showing the sisto-diastolic excursions, while keeping the spatial relationships. 65 normal subjects were studied and 4 motion patterns were identified: parietal muscular, parietal vascular, atrio-ventricular valvular and aortic valvular.
The clinical application of a new ultrasonic technique, echocardiokymography (ECKG), has been showed particularly useful in the detection of myocardial and pericardial dyskinesias. In patients with congestive cardiomyopathy, the global hypokynesia was confirmed by the ECKG; regional impairment of parietal wall motion after myocardial infarction is clearly demonstrated by the technique; acute and chronic pericarditis show peculiar kymographic patterns. The ECKG is a kind of two-dimensional examination, that keeps some of the advantages of the time-motion, in the comparative study of cardiac walls dynamics.
The diagnosis of tricuspid regurgitation (TR) is often controversial. We used peripheral venous contrast echocardiography for the detection and the quantitative assessment of valvular regurgitation. We studied 10 normal subjects, 7 patients with atrial fibrillation, but without tricuspid lesions, 36 patients with TR confirmed by right heart catheterization, divided in three subgroups, according to ventriculography and jugular pulse recording: 10 cases with mild TR, 17 cases with moderate TR, 9 with severe regurgitation. After the injection of contrast medium (CM) (saline solution), the regurgitant flow was visualized in the hepatic veins (HV) and in the inferior vena cava (IVC), by two-dimensional subxiphoid projections; the time of disappearance of the CM was studied by time-motion echograms. The appearance of CM in the HV and in IVC wasn't demonstrated in any normal case. Subjects with atrial fibrillation alone, showed, in 71,5% of cases of persistence of CM in IVC for less than 10 cardiac beats. The diagnosis of severe TR was correctly made in 100% of cases; in all the patients the CM was showed in the HV for more than 40 beats. In patients with mild TR, the diagnosis was correct in 60% of cases with a short persistence of the CM in the HV. In the other cases of mild TR, the presence of CM in HV was misinterpreted as due to atrial fibrillation. Moderate TR was correctly recognized in 70.5% of patients, while in the remainder it was under or overestimated. The method shows a good sensitivity; some cases with atrial fibrillation, in the absence of TR, may cause "false-positive" diagnosis.
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Twenty patients varying in age between 5 and 20 years at the time of surgical closure of VSD were studied 2 to 9 years postoperatively. Ventricular function was studied by echocardiography and measurement of systolic time intervals for the left and right ventricles and the findings were related to clinical and haemodynamic results of operation. The VSD was closed in all instances and the haemodynamic situation was normalized in all but 2 patients who had persisting pulmonary vascular disease. Right bundle branch block (RBBB) was recorded in 11 instances and in 5 there was an associated left axis deviation (LAD), suggesting left anterior hemiblock. LAD occurred as an isolated anomaly in another 2 patients. The heart size was within normal limits in all the patients. Abnormal septal motion (ASM) was recorded in 13 of the 20 patients, but other echocardiographic analyses, such as LV end-diastolic dimension, left atrial/aortic root ratio, posterior wall velocity index and maximal endocardial velocity, were all within predicted normal limits. There was an almost uniform prolongation of both left and right pre-ejection periods. left and right ejection period as a rule remained normal and gave an increased PEP/ET ratio, indicating the presence of postoperative ventricular dysfunction also in instances with complete normalization of the haemodynamic situation. Suggested background mechanisms for these findings are the frequent occurrence of conduction defects postoperatively, the likelihood of altered ventricular compliance and possibly also as a cause of ASM postoperative presence of an opened pericardial sac.
Peripheral venous contrast echocardiography is an established method in the assessment of cyanotic congenital heart diseases and for the exact definition of the inner cardiac surfaces outlines. We found it extremely useful in order to correctly delineate the right border of the interventricular septum in IHSS. The method showed that the interventricular system thickness had been underestimated in five out of six patients.
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Three patients with corrected transposition of the great arteries (CTGA) have been studied by means of single plane (M-mode) and two-dimensional (2-D) echocardiography: the first study was performed after surgical closure of a VSD and the remaining two before cardiac catheterization. The following M-mode findings can suggest the diagnosis in CTGA: the interventricular septum (IVS) may not be visualized, there is lack of continuity between the posterior a-v valve (tricuspid) echoes and the anterior great artery (aorta), the posterior a-v valve leaflets may show some abnormalities in shape. The measurement of systolic time intervals of both semilunar valves can help in distinguishing the pulmonary artery from the aorta; further information can be obtained by means of peripheral venous contrast injection, which, in absence of right-to-left shunt, opacifies the posterior great vessel (pulmonary). The 2-D view of the heart allows the identification of the morphological type of ventricle and of the spatial great arteries relationship. The posteriorly and left located ventricle is recognized as morphologically right, because of the tricuspidal shape of its a-v valve: its attachment to IVS is lower than that of the mitral valve (4-chambers view) and three leaflets may be evident (short-axis); 3 papillary muscles and gross trabeculations can be identified (short axis and 4-chambers views, respectively). In long-axis the anterior vessel (aorta) runs parallel to the sternum; in short-axis both vessels are imaged as adjacent circles; by means of peripheral contrast injection, in conditions without right-to-left-shunt, the right and posterior vessel is recognized as a pulmonary artery. The differential diagnosis is discussed with d-transposition, Fallot's tetralogy, Taussig-Bing anomaly, common trunk, univentricular heart. According to our experience, the diagnosis of CTGA and associated defects can be made by M-mode and 2-D echocardiography.
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Seven patients with hemodynamic and angiocardiographic diagnosis of supravalvular aortic stenosis were studied by single plane echocardiography. 3 patients had the hypoplastic and 3 the "hourglass" type of the disease. 3 patients underwent surgical repair of the malformation, with postoperative echocardiographic control. There was no relationship between the lumen dimension variations as measured by echocardiography and the transtenotic pressure gradient. With respect to angiocardiography, echocardiography underestimates the severity of the disease. The method was always diagnostic, but the anatomic type of stenosis could not be determined. The severity of the disease can be only indirectly assessed by evaluating left ventricular hypertrophy induced by pressure overload.