[Vasodilators: which, how, when].
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Biomedical subjects
Publications and source records attributed to L Mestroni.
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Sixty-five patients with dilated cardiomyopathy were studied by means of 24-hour ECG monitoring. Ventricular arrhythmias were present in 62 (95.4%), of whom 52 (80%) showed a complex form (multiform ventricular extrasystoles, pairs, and ventricular tachycardia). Forty-one patients, presenting with complex ventricular arrhythmias, received antiarrhythmic treatment with amiodarone (600 mg/day in the first week, 400 mg/day in the second week, and 200 to 400 mg/day chronically), and were then controlled with periodic 24-hour ambulatory monitoring. A significant reduction in the number of ventricular extrasystoles was seen in over 70% of patients during a 3-year period. There was also a significant decrease in the incidence of complex ventricular arrhythmias (particularly of ventricular tachycardia). Adverse effects were noted in 23 patients, but only four had to stop treatment. During the follow-up period, 19 patients died: 14 of heart failure, four of sudden death, and one of a noncardiac cause; all patients who died suddenly were not treated with amiodarone (p = 0.022). Complex ventricular arrhythmias are frequent in dilated cardiomyopathy and it is suggested that amiodarone is effective in short- and long-term control of these arrhythmias.
Aim of this study is the analysis of clinical, morphologic and haemodynamic features of cardiac amyloidosis. Cardiac amyloidosis was demonstrated histologically in 7 of our patients: in 6 by endomyocardial biopsy during cardiac catheterization, in one at autopsy. The clinical picture was characterized in every patient by signs and symptoms of congestive heart failure. The electrocardiogram showed several non specific signs: low voltage of the QRS complexes, both in peripheral (4/7) and precordial leads (7/7 cases); marked leftward and upward deviation of the QRS axis (6/7 cases); first degree A-V block (5/7); abnormal Q waves (7/7). M-mode and two-dimensional echocardiography invariably demonstrated a typical pattern: a non dilated left ventricle with thickened and hyper-refractile walls, and usually a slight-moderate diffuse hypokinesia. Other common features were a thickening of right ventricular walls, interatrial septum, and atrioventricular and semilunar valves. Computerized analysis of the M-mode tracings disclosed a marked impairment of the indexes of both systolic and diastolic ventricular function in all patients. By correlating electrocardiographic and echocardiographic data, we found in every case a striking disproportion between the low QRS voltage and the high muscle cross-sectional area (an echocardiographic index of left ventricular mass): this pattern appears to be highly suggestive of infiltrative heart disease. Cardiac catheterization (performed in 6 cases) showed an increase of left ventricular (6/6) and right ventricular (5/6) end-diastolic pressure, with a dip plateau pattern in some cases (4/6 of the left, 2/6 in the right ventricle). The cardiac index was decreased in 3/6 cases. Left ventricular angiography confirmed the echocardiographic data of normal volumes and a slight-moderate decrease of the ejection fraction. We conclude that cardiac amyloidosis usually mimics a restrictive cardiomyopathy (severe congestive heart failure with increased ventricular filling pressures, in the absence of severe systolic ventricular dysfunction). This disease can be suspected clinically by the correlation of the clinical, electrocardiographic and echocardiographic data. The final diagnosis requires an endomyocardial biopsy.
DILATED CARDIOMYOPATHY - Conduction and rhythm disturbances are frequent findings in dilated cardiomyopathy. 65 patients with dilated cardiomyopathy underwent 24-hour electrocardiographic monitoring: 95.4% showed ventricular arrhythmias, 80% complex ventricular arrhythmias and 44% runs of non-sustained ventricular tachycardia. Over 1000 ventricular extrasystoles in 24 hours were present in 44% of cases. Ventricular tachycardia and multiform and paired ventricular extrasystoles correlated significantly with the severity of cardiac dysfunction and with a worse prognosis. Patients undergoing antiarrhythmic therapy (amiodarone) showed a significant reduction in the number of ventricular extrasystoles and in the incidence of complex ventricular arrhythmias. HYPERTROPHIC CARDIOMYOPATHY - The high incidence of arrhythmias, particularly ventricular arrhythmias (approx. 70% of cases) in hypertrophic cardiomyopathy is well recognized: episodes of ventricular tachycardia are present in 20% of cases and are related to an elevated risk of sudden death. Antiarrhythmic treatment with amiodarone significantly reduces the number of ventricular extrasystoles and the episodes of ventricular tachycardia, may prevent sudden death and improve survival. RESTRICTIVE CARDIOMYOPATHY - Very little information is present in literature concerning this extremely rare form, in which every type of rhythm and conduction disturbance has been observed. CONCLUSIONS - Electrocardiographic monitoring is nowadays a very important tool in the management of cardiomyopathy patients, to identify possible patients at risk and to monitor the antiarrhythmic treatment.
Sixty-five patients with dilated cardiomyopathy underwent 24 hour electrocardiographic monitoring: 62 (95.4%) showed ventricular arrhythmias and 52 (80%) complex ventricular arrhythmias (multiform ventricular extrasystoles, paired ventricular extrasystoles and ventricular tachycardia). Complex ventricular arrhythmias correlated significantly with some haemodynamic indices of ventricular dysfunction: patients with multiform and paired ventricular extrasystoles and with ventricular tachycardia had lower values of ejection fraction (31.9 +/- 11.8%, P = 0.002) and of cardiac index (2.9 +/- 0.7 litres/min/m2, P = 0.029) than the others (41.1 11.1% and 3.5 +/- 0.9 litres/min/m2 respectively). Patients were followed for a period of 30 +/- 18 months (20 days to 64 months). During follow-up 19 died and mortality was higher among patients with multiform and paired ventricular extrasystoles and/or ventricular tachycardia. Complex ventricular arrhythmias are frequent in dilated cardiomyopathy: ventricular tachycardia and multiform and paired ventricular extrasystoles seem to be related to a more depressed ventricular function and to a poor prognosis. The importance of antiarrhythmic treatment in these patients has still to be evaluated.
The electrocardiogram (ECG) of 80 patients with dilated cardiomyopathy was studied. An abnormal ECG was present in 100% of our patients, and in 25% it was the first sign of the disease. Thirty-eight cases (47.5%) showed left atrial enlargement, 22 (27.5%) prolonged PR interval, 33 (41.2%) left bundle branch block, 15 (18.7%) abnormal Q waves, 9 (11.2%) primary S-T and T changes. There were significant differences in ejection fraction and in left ventricular end-diastolic volume between patients with right bundle branch block (p less than 0.05 and p = 0.05 respectively). Patients were followed for a period of 29.5 +/- 28.8 months (min. 2 days, max. 10 years): during the observation period the ECG showed in 28 cases an increasing left ventricular conduction delay and a leftward shifting of mean QRS axis. Patients with left ventricular conduction delays showed a worse prognosis. ECG in dilated cardiomyopathy is a nonspecific but sensitive tool, which may be related to different degrees of myocardial impairment and may be useful in the definition of a prognostic profile.
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Thirty patients with congestive cardiomyopathy (C.C.) have been studied for the prevalence of neutralizing antibodies to coxsackie B viruses in comparison with age and sex matched controls. Seropositivity toward each antigen was similar in cases and controls: an exception was coxsackie B5 virus, where a significantly seropositivity was found in the control group. As a whole, high antibody titers to any antigen were observed more frequently on sera of cardiopathic patients; however the difference between cases and controls of g.m.t. to each antigen tested was not statistically significant, with the exception of coxsackie B1 virus. The absence of a clear relationship between C.C. and viral infections might be explained through biological as well as epidemiological considerations; of particular relevance, the long duration of cardiac disease (average length 71 months, median 54). Final considerations are offered regarding the methodologic approach for a better understanding of the etiology of this elusive disease.
Vasodilator drugs are generally classified according to their prevalent site of action: arteriolar vasodilators (e.g. phentolamine, hydralazine, nifedipine) which reduce peripheral resistance and, therefore, increase stroke volume and cardiac output; venodilators (e.g. nitrates), which decrease filling pressure, redistributing intravascular blood volume from the central to the peripheral reservoirs and therefore relieve signs and symptoms of congestion; "balanced" vasodilators (e.g. nitroprusside, prazosin, captopril) which present both effects. Vasodilator therapy is indicated in heart failure caused by impaired contractility (congestive cardiomyopathy, ischemic heart disease) and volume overload (mitral and aortic regurgitation, ventricular septal defect). Hemodynamic studies of acute pharmacological effects are necessary for a correct drug choice, even if they are not always predictive of the long-term efficacy. Non-invasive studies (in particular echocardiography) don't seem actually adequate for vasodilator therapy evaluation. Finally it is not known if vasodilator treatment influence prognosis of chronic heart failure (especially survival), but there is evidence that it can lessen symptoms and increase effort tolerance.
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Acute and chronic effects of captopril (C) were studied in 14 patients (12 males, 2 females; mean age 56 +/- 15 years) with chronic congestive heart failure (CCHF) refractory to digitalis and diuretics. All patients underwent hemodynamic evaluation before and after increasing doses of C (6.25-100 mg). Nine patients were evaluated during long term therapy by means of clinical examination, exercise testing, chest-X-ray and echocardiography. After C the following acute haemodynamic changes were observed. Mean right atrial pressure: -25% (p less than 0.01), left ventricular filling pressure: -22% (p less than 0.01), mean systemic arterial pressure: -15% (p less than 0.01), systemic vascular resistance: -31% (p less than 0.01), cardiac index: +36% (p less than 0.01). Of the 9 patients who were evaluated during long term C treatment, 7 (group A, mean follow up 6.4 +/- 4.2 months) improved in 1 or 2 NYHA functional classes and showed an increased exercise tolerance during the first 3-6 months of therapy. In this period, however, two sudden deaths and one drop-out were observed. Moreover, after the seventh month two patients of this group deteriorated clinically. Two patients (group B) developed a progressively weight gain during the first 15 days of C treatment. In the majority of our patients with refractory CCHF, captopril improves cardiac performance in the acute phase and in the first 3-6 months of therapy. Controlled studies and longer follow up are needed to understand better the long term effects of C in CCHF patients.