L-Carnitine treatment initiated early after acute myocardial infarction and continued for 12 months can attenuate left ventricular dilation during the first year after an acute myocardial infarction, resulting in smaller left ventricular volumes at 3, 6 and 12 months after the emergent event.

Fatty acids accumulate in the muscle cells in some carnitine deficiency syndromes due to a variety of genetic defects in intermediary metabolism. L-Carnitine administration may relieve this excess by transporting acyl compounds out of the cell as acylcarnitine. Similar fatty acid accumulation occurs during myocardial ischaemia because of the decreased rate of beta-oxidation, and this has been put forward as a cause of ventricular arrhythmias. This study was carried out to investigate whether administration of high doses of i.v. L-carnitine in patients with acute myocardial infarction could increase urinary excretion of acylcarnitine and reduce early ventricular arrhythmias. Fifty-six patients suffering from acute myocardial infarction, admitted to the Coronary Unit between 3 and 12 h after the onset of symptoms, were included in the study. The design of the study was double blind, parallel and placebo controlled. Allocation of treatment to patients was done randomly after stratification (time from onset of pain and site of infarction). The first group (28 patients) received intravenous L-carnitine at a dose of 100 mg kg-1 b.w. every 12 h for 36 h while the second group (28 patients) received placebo intravenously. Immediately before starting treatment two blood samples were taken (at 5-min intervals) and a further 16 samples were taken at regular intervals over the following 48 h. Patients' urine was collected over the same period of time. Concentrations of free carnitine, short chain acylcarnitine esters and long chain acylcarnitine esters in serum and urine were measured.(ABSTRACT TRUNCATED AT 250 WORDS)

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In order to assess the respective values of two-dimensional echocardiography (2D echo) and computed tomography (CT) in the evaluation of aneurysms of the thoracic aorta, 14 patients with angiographically proven aneurysms of the thoracic aorta (three of which were dissecting aneurysms) were studied. The entire thoracic aorta was visualized in 10/14 patients by 2D Echo and in all patients by CT. An intimal flap was recognized by 2D echo in each case with a dissection whereas such a recognition was never possible with CT. CT identified calcification of the wall of an huge aneurysm of the ascending aorta in one case and a thrombotic stratification in the lumen of the descending thoracic aorta in another case; both abnormalities were missed by echocardiography probably because of inappropriate gain setting. In conclusion, 2D Echo and CT are both useful in the evaluation of aneurysms of the thoracic aorta; 2D echo appears to be superior in the recognition of an intimal flap due to dissection whereas CT allows a better recognition of the configuration, extension and tissue modifications of the aneurysm.

Evidence has recently been produced to show that patients with a midsystolic click and late systolic murmur have a peculiar abnormality of the mitral valve: the systolic ballooning of the leaflets, particularly the posterior one, usually associated with mild mitral insufficiency. Occurrence of similar clinical, phonocardiographic, and electrocardiographic findings in more than one member of each of eight families studied strongly supports the hypothesis of a genetic basis. The frequent association with findings indicating myocardial involvement is pointed out. Its potential aetiological implications are discussed. The possible links with the forme fruste of the Marfan syndrome are also considered. Some distinctive clinical, phonocardiographic, and electrocardiographic features are described.