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Patients with catheter fragments that were entrapped during percutaneous transluminal coronary angioplasty remain a particular challenge because little is known about the clinical outcome. Absolutely unique is the partially cutting of the dilator and the pushing of the fragment by the guidewire advancing into the femoral artery to the coronary tree. We describe this exceptionally complication with a complete coronary obstruction and an anterior myocardial infarction sustained by the retained fragment into the left main branch., (Copyright © 2009 Elsevier Ireland Ltd. All rights reserved.)

The cardiovascular manifestations of tetanus consist of disturbances of heart rate and rhythm, blood pressure instability, arrhythmias, myocardial dysfunction and sympathetic overactivity. It was suggested that either a sudden loss of catecholamine stimulation or myocardial damage caused by the direct action of the tetanus toxin, could be involved in cardiac dysfunction described in tetanus. However, histologic evidence of myocardial necrosis in tetanus was demonstrated in few cases. We report a fatal case of tetanus in which we investigated the cardiac morphology and the expression of TNFalpha to elucidate the heart involvement in this case. Since it is well known that myocardial damage caused by catecholamines can induce synthesis of cytokines by myocytes, cytokines, specifically those with known cardiodepressant properties such as TNF-alpha, could be an alternative mechanism involved in cardiac dysfunction in the setting of tetanus.

During the clinical course of dilated cardiomyopathy, arrhythmias, thromboembolism and sudden death are common and may occur at any stage. In patients with dilated cardiomyopathy, elevated plasma levels of tumor necrosis factor-alpha are associated with poor prognosis. In animal experiments and clinical trials, myocardial tumor necrosis factor-alpha expression correlates with increased mortality rates. A case of sudden death of a previously asymptomatic young man, having a definitive autoptic diagnosis of dilated cardiomyopathy with endomyoelastofibrosis, is presented. We investigated the cardiac morphology and the expression of tumor necrosis factor-alpha in cardiac tissue specimens to elucidate the role of tumor necrosis factor-alpha expression in this fatal case. Our results demonstrate a strong positive myocytes reaction for tumor necrosis factor-alpha in the heart specimens. The pathogenesis of the fatal event is discussed with particular reference to the histological findings and myocytes expression of tumor necrosis factor-alpha.

Symptoms of cardiac contusion are very greatly and sometimes are non recognized or are masked by associated injury in severe chest trauma. Cardiac contusion clinically presents as a spectrum of signs and symptoms of varying severity, ranging from precordial pain, dyspnoea, and non specific ECG changes to increased serum activity of several enzymes, early severe rhythm abnormalities, severe conduction defects and death. We present a fatal case in which the definitive diagnosis of myocardial contusion has proved complex. All clinical data were suggestive of acute myocardial infarction, but the history of chest wall injury and gross and histological examination of the heart and coronary vessels led us to conclude for a cardiac contusion without myocardial infarction. In case of chest blunt trauma, the ECG should be interpreted within the context of the clinical situation, on history of chest wall injury, since a fatal myocardial contusion may occur after apparently mild injury.

Authors present the case of the sudden death of a 30-year-old man, 3 h since his hospitalization by the onset of aspecific chest pain. ECG findings revealed the presence of localized ST segment elevation in precordial leads (V1-V4) and DII-DII, and aVF mimicking acute antero-inferior myocardial infarction. A diagnosis of acute antero-inferior myocardial infarction was advanced and the patient introduced to thrombolytic therapy. Suddenly, on ECG monitor, conduction abnormalities were early recorded (ventricular extrasystole) followed by ventricular tachycardia degenerating in fatal ventricular fibrillation. An alleged medical malpractice was sued against the cardiologist. A complete immunohistochemical study was performed. Histologically, the heart presented massive interstitial lymphocytic infiltrate and focal myocytes necrosis. The diagnosis of acute lymphocytic myocarditis was established as the cause of death.