[Cardiotoxicity induced by radiotherapy]. / Cardiotossicità da radioterapia.

The correct diagnosis of radiation-associated cardiac disease is mandatory to avoid useless surgical treatment. We report one patient who underwent mitral replacement and right coronary revascularization thirteen years after radiant therapy for breast cancer.

[False chordae tendineae]. / Le false corde tendinee.

False tendons (FT) are fibrous or fibromuscular structures which cross the ventricular cavity with no connections with valvular leaflets. They were considered for a long time as normal structures but now cardiologists are interested because of the possible association with the so-called innocent murmur, and even more so for the role they can have in eliciting ventricular arrhythmias. Some Authors believe that arrhythmias can arise from the false tendons because they contain not only fibrous tissue but also muscular and conduction tissue. Arrhythmias can be triggered either by stretching of the Purkinje fibers or by distortion of the ventricular wall, where false tendons arise. At the same time they can act as reentry circuits due to their non-homogeneous structure. Due to the fact that false tendons may arise anywhere from the ventricular cavity, they have been classified according either to anatomic or echocardiographic criteria: the latter being more complex and difficult than the former for the difficulty in locating the attachment areas. In our echocardiographic laboratory we simply distinguish two types of false tendons: type I which parallel the interventricular septum or bridges from the postero-basal portion of the septum to the posterior left ventricular wall; type II which crosses the ventricular cavity more distally, towards the apex. In the anatomic studies the prevalence of the FT is rather homogeneous, ranging from 46 to 54.9%, while it is extremely variable in the echocardiographic studies, ranging from 0.2 to 71%. This is possibly due not only to the examiner's skills, or the equipment's quality but also to the population studied. Among the patients referred to our cardiac paediatric unit we have found false tendons in 80 (29.3%) out of 273 children without cardiac disease, age ranging from i day to 13 yrs. Males were affected twice more than females, 63.7% vs 36.3%.(ABSTRACT TRUNCATED AT 250 WORDS)

Isolated hypertensive lower esophageal sphincter. Clinical and manometric aspects of an uncommon esophageal motor abnormality.

The hypertensive lower esophageal sphincter is an infrequent primary esophageal motor disorder characterized by elevated mean lower esophageal sphincter pressure (greater than or equal to 3 SD from that of controls), sphincter relaxations greater than 75%, and normal peristaltic activity in the esophageal body. This disorder is frequently associated with the nutcracker esophagus. We report our clinical and manometric experience with the isolated hypertensive lower esophageal sphincter (i.e., unassociated with other motor disorders), which constituted 2.7% of all patients who complained of dysphagia or chest pain referred for manometry during the period from October 1982 to February 1991.

[Mitral valve prolapse and endocarditis prophylaxis]. / Prolasso della valvola mitrale e profilassi della endocardite.

This paper briefly reviews the anatomy, epidemiology and clinical aspects of the Mitral Valve Prolapse (MVP), and focuses attention on the association between infective endocarditis and prolapse, particularly after oral surgery. It is recommended that all MVP patients, irrespective of whether they have mitral regurgitation or not, receive correct prophylactic treatment. The pharmacological approach suggested, based on the most recent advances in antibiotic pharmacodynamics, is designed in accordance with specific patient risks.

Comparative effects of ibopamine and captopril in mild congestive heart failure. Focus on the long-term effects of inodilation on ventricular arrhythmias.

Twenty-three patients with mild heart failure (I-II NYHA classes) on digitalis and diuretics were assigned to the following treatment in a random and double-blind fashion: ibopamine-captopril, ibopamine-placebo, captopril-placebo, and placebo-placebo. The doses of captopril and ibopamine were respectively 25 mg t.i.d. and 100 mg t.i.d. The incremental exercise time (until exhaustion) and the peak VO2 (oxygen consumption), the indexes of left ventricular function (by echo and nuclear stethoscope) and ventricular arrhythmias (evaluated by prolonged Holter monitoring) were assessed before randomization, at 45 days and at 3 months. Ejection fraction, exercise time, peak VO2, ventricular arrhythmias and heart rate (at rest and during exercise) appeared to be equally unaffected by each treatment. Our results show that ibopamine exerts no significant effects on either heart rate or ventricular arrhythmias and that indexes of left ventricular function are not modified by any treatment in mild congestive heart failure.

Sympathetic activation on effort in patients with chronic heart failure. Long term effects of captopril.

Ten patients with congestive heart failure (CHF) (NYHA II-IV) on adjusted doses of digitalis and diuretics underwent a careful clinical assessment including an evaluation of exertion dyspnoea and the usual echocardiographic indices of cardiac performance. A cardiopulmonary exercise test with an increment of 20W every 3 minutes was prolonged until exhaustion. Systemic arterial pressure, ECG, VO2, VCO2 and VE were monitored throughout. Gas tensions, plasma catecholamines and lactate were measured in blood samples taken at the first and third minute of each exercise stage. The above measurements were carried out before and after 3 months of treatment with Captopril, 50 mg b.i.d. or t.i.d. A highly significant correlation between arterial lactate and plasma norepinephrine (NE) was observed in each patient during both exercise tests (r = 0.77 to 0.99; p less than 0.05 at least). Left ventricular end-diastolic dimensions were reduced by Captopril (from 69.9 +/- 1.7 to 65.2 +/- 1.4 mm, p less than 0.01) along with a concomitant increase in percent fractional shortening. Most of the patients were reclassified at a lower NYHA class and a significant decrease in dyspnoea score was observed. The exercise time was significantly increased (from 11.2 +/- 1.8 to 12.9 +/- 1.9 min; p less than 0.05), but the peak values of NE, arterial lactate and VO2 were not affected by the treatment. The predicted value of VE at a VCO2 of 1 L/min, regarded as an index of dyspnoea, was significantly decreased by Captopril (from 41.4 +/- 2.9 to 38.9 +/- 2.7 L/min; p less than 0.05). The positive effects of long-term treatment with Captopril on cardiac performance in CHF are confirmed. Sympathetic activity is linked to anaerobic muscular metabolism during exercise and seems to be independent of pharmacological ACE inhibition. The discrepancy between the exercise tolerance and the peak VO2 might be explained by a better utilization of the available energy.

Acute left ventricular filling time and rate changes in hypertrophic cardiomyopathy after verapamil and propranolol evaluated by nuclear stethoscope.

We have undertaken the present study to evaluate the acute effects of propranolol and verapamil on the diastolic function in patients with hypertrophic cardiomyopathy. We used a non imaging isotope device, the nuclear stethoscope, that has been so far mainly employed for assessment of systolic function, although fitted for detecting diastolic filling rates and times as well. Relative cardiac output, ejection fraction, rapid and slow filling times and rates were measured in five patients suffering from hypertrophic cardiomyopathy in basal conditions and 10.20 and 30 minutes after i.v. administration for either propranolol or verapamil, with a time interval of at least 24 hours between the two acute drug studies. With respect to the baseline values only verapamil showed a significant improvement in rapid and maximum filling rates, suggesting that diastolic function is more beneficially affected by Ca-entry blockers rather than beta-blockers in hypertrophic cardiomyopathy.

Acute effects of captopril in hypoxic pulmonary hypertension. Comparison with transient oxygen administration.

The present study was carried out to test the hypothesis of a possible effectiveness of captopril--an enzymatic inhibitor of both angiotensin II formation and bradykinin degradation--on hypoxic pulmonary hypertension. In 6 patients with this clinical condition, captopril-induced changes in pulmonary hemodynamics were observed after the acute administration of the drug with and without a short period of oxygen therapy at a flow rate sufficient to keep the PaO2 over 60 mm Hg. In our patients, captopril significantly lowered pulmonary arterial pressure and vascular resistance only when combined with oxygen, suggesting that an increase in bradykinin availability and/or a decrease in angiotensin II synthesis might be important factors in reversing pulmonary arterial hypertension only after blunting of the hypoxic stimulus on pulmonary circulation. Moreover, the authors suggest that the employment of vasodilators in the setting of hypoxic pulmonary hypertension should be considered not only as a means of relieving vasoconstriction but also as a possible tool for maintaining cardiac output and, in turn, peripheral oxygen delivery.

Efficacy of two different doses of muzolimine in the treatment of mild hypertension.

UNLABELLED: A report is given on the effects of oral therapy with muzolimine (M) in patients with mild hypertension. SUBJECTS AND METHOD: 21 untreated patients, aged 35 to 69 (mean 53.1 yrs) with orthostatic diastolic BP between 100 and 115 mmHg were randomly assigned to either group A (10 mg M/day) or group B (20 mg M/day) in a single blind study for a period of two weeks. Clinostatic and orthostatic systolic and diastolic BP and heart rate were recorded at weekly intervals. PRA, aldosteronemia, ECG and blood chemistry were analyzed at the beginning and at the end of the study. Student's t-test was used for the statistical evaluation and p values below 0.05 were considered significant. RESULTS: Both clinostatic and orthostatic diastolic BP were significantly reduced in group A whereas only orthostatic diastolic BP was decreased in group B (Fig. 1). PRA and aldosteronemia values and blood chemistry showed no statistically significant changes. No side effects were noted. We conclude that 10 mg/day of muzolimine is more effective than 20 mg/day in reducing orthostatic diastolic BP (A vs. B p less than 0.02). Although these results are only preliminary data and further investigations are required, they suggest that muzolimine may be safely used, in combination with other antihypertensive agents, particularly in cases of renal failure.