[Atrial natriuretic factor in patients with cardiac decompensation before and after chronic therapy with an angiotensin-converting enzyme inhibitor]. / Fattore natriuretico atriale in pazienti con scompenso cardiaco prima e dopo terapia cronica con un inibitore dell'enzima di conversione.

BACKGROUND: Patients with severe congestive heart failure often have high plasma Atrial Natriuretic Factor (ANF) and neurohormonal activation. Ace inhibitors give clinical and hemodynamic benefits and lower plasma angiotensin and norepinephrine levels. The interactions between ANF and the Ace inhibitors are mainly modulated via the renin angiotensin system. METHODS: Plasma ANF, renin activity, urinary aldosterone and catecholamine levels were evaluated in 10 patients with congestive heart failure (at baseline, after 15 days of adequate treatment with digoxin and diuretics, and after 45 days of enalapril) in order to assess the changes of ANF and vasoconstrictor neurohormones with chronic Ace inhibitor therapy. RESULTS: ANF increased significantly in the congestive heart failure group compared to a normal subject control group (P < 0.001). After digoxin and diuretic therapy NHYA class improved significantly, but no significant hormonal changes were found. On the contrary, the addition of enalapril caused a significant decrease of plasma ANF and urinary aldosterone and catecholamines (P < 0.05). CONCLUSIONS: The relationship between the renin angiotensin system and catecholamines is complex but our findings indicate that: 1) Traditional therapy is effective in improving symptoms, but cannot induce a decrease of vasoconstrictive neurohormones; 2) ACE inhibitor therapy reduces ANF and neurohormonal activation. 3) ANF is a useful marker in evaluating the response to treatment.

Reduction of complex ventricular arrhythmias after enalapril treatment in patients with advanced stable heart failure.

We studied, by 48-hour Holter monitoring, 33 patients with chronic stable heart failure (radionuclide ejection fraction less than 35%), complex ventricular arrhythmias and no electrolyte abnormalities, after a period during which they were treated with digoxin and diuretics. Before Holter monitoring blood samples were analyzed for serum concentration of sodium, potassium, magnesium, urea, creatinine, digoxin, aldosterone and for plasmatic renin activity in addition to urinary aldosterone and catecholamines determination. After these investigations in 23 patients, 5-20 mg of enalapril were progressively added to the conventional therapy, while 10 patients continued the previous therapy. After 8 weeks 30 patients were subjected to a second 48-hour Holter monitoring and to the same biochemical and hormonal tests. One patient died and 2 were lost to follow up. Only the enalapril group showed a significant decrease in the number of premature ventricular complexes (PVC) (p less than 0.01), and the frequency of couplets and episodes of ventricular tachycardia (VT) declined significantly (P less than 0.01). In the two groups there were no significant changes in digoxin, sodium, or magnesium, while potassium concentration increased in both groups (p less than 0.01). In the enalapril group heart rate and systolic and diastolic pressure declined significantly (p less than 0.01), and New York Heart Association class (NYHA) improved (p less than 0.001). In the other group there were no significant changes in these parameters. Enalapril caused a significant increase in the plasmatic renin activity (p less than 0.01) and a significant fall of plasma and urinary aldosterone (p less than 0.01; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

[Correlation between QT interval, ventricular arrhythmias and left ventricular function in chronic alcoholics]. / Correlazione tra l'intervallo QT, le aritmie ventricolari e la funzione ventricolare sinistra negli etilisti cronici.

Prolonged QT interval and arrhythmias have been reported to occur in chronic alcoholics. To investigate the role of chronic alcohol consumption in the onset of arrhythmias and the development of the preclinical left ventricular dysfunction, in a group of 12 asymptomatic chronic alcoholics with no clinical evidence of heart disease, with histologically proven hepatic damage, after a week of abstinence from alcohol, the following investigations were performed: measurements of the corrected QT interval (QTc), 24-hours Holter monitoring, systolic time intervals, M-mode echocardiograms. The results were compared to those of 10 normal subjects. Our data suggested no difference in QTc interval between chronic alcoholics and normal persons. The distribution of arrhythmias was not statistically different in the two groups, particularly frequent and complicated arrhythmias occurred in only one subject in each group. Preejection period corrected for heart rate (PEPI) was significantly longer in alcoholics (132 +/- 16 vs 119 +/- 11, p less than 0.05). All echocardiographic parameters examined were not significantly different in the two groups. On the basis of our results, our impression is that the arrhythmogenic role of alcohol, not under acute ingestion, is relatively unimportant and further studies are needed to become a definitive conclusion about subclinical alcoholic cardiomyopathy.