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Background: The aim of the present study was to investigate the relationship between carotid and aortic atherosclerosis in asymptomatic subjects., Methods: Eighty-three consecutive patients without history of cardio- and cerebrovascular disease, referred for transesophageal echocardiography, were enrolled into the study., Results: Aortic plaques were found in 40 out of 83 patients, whereas carotid atherosclerosis was present in 43% of the entire study population and in 75% of patients with aortic atherosclerosis (30 out of 40 patients). At multivariate logistic analysis, the presence of carotid atherosclerosis was a predictor of aortic atheroma, independently of traditional risk factors., Conclusions: In asymptomatic patients, aortic plaque occurrence may reflect the presence of carotid plaques and an ultrasound assessment should be advised.

Approximately 25% of cerebral infarction is cardioembolic in nature. Transoesophageal echocardiography is widely regarded as the initial study of choice for evaluating cardiac source of embolism. We studied the records of 83 consecutive patients referred to our Neurologic Ward between January 2000 and October 2006 with diagnosis of ischemic cerebrovascular disease of unknown cause (cryptogenetic strokes). A potential cardiac of emboli source was found in 36.1% of the patients. Atrial septal abnormalities and aortic plaques accounted for most of the detected findings. Our experience suggests that routine transoesophageal echocardiography in this setting is of value and has a high impact on clinical management.

Numerous and extremely varied conditions (intense muscular activity, ischemia, metabolic and genetic disorders, infections, immunological diseases and toxic causes) may play a role in the genesis of non-traumatic rhabdomyolysis. Over the past years there has been an increased number of reports of forms due to drug or narcotic intoxication. Seven cases of rhabdomyolysis are reported in patients admitted to emergency wards in a state of coma due to heroin overdose (4 cases), cocaine overdose (1 case), carbamazepin (1 case), and tricyclic anti-depressives (1 case). In all cases it was possible to hypothesise a multifactorial pathogenesis of the disease in which other factors, such as acidosis, hypoxia, hypothermia and compression of the muscle mass during coma, were associated with the direct toxic damage caused by the drug. The most frequent complication was acute renal failure. One case of myocardial involvement with non-Q infarction characteristics was also observed.

It is well known that heroin overdose may cause rhabdomyolysis. Sometimes a myocardial involvement complicates its course. We report a case of heroin intoxication followed by rhabdomyolysis associated with myocardial injury, with symptoms, laboratory findings, ECG and echocardiography features of non-Q wave infarction. However, a 201 Tl myocardial scintigraphy, performed after patient discharging, did not show any abnormality. We think that heroin has a direct myotoxic effect on both myocardium and skeletal muscle. Yet we cannot exclude that hypoxia, acidosis, vasoconstrictive substances released by muscle necrosis, or hypersensitivity reactions associated with heroin or some of its adulterants are involved in myocardial injury.