The present study focuses on the application of a therapeutic strategy in patients with chronic severe lower limb ischaemia using a plasmid vector encoding the vascular endothelial growth factor (phVEGF165). It has been shown that VEGF promotes neo-vascularization and blood vessel network formation and thus might have the ability to improve blood-flow at the level of the affected limbs. However, little information is available regarding the necessary level of expression of VEGF and its possible related adverse effects. We have subcloned VEGF
165isoform into pCMV-Script expression vector (Stratagene) under the control of the CMV promoter. Three patients with chronic ischaemia of the lower limb, considered as not suitable for surgical re-vascularization, received intramuscular injection with 0.5 ml saline solution containing 1011 copies of VEGF
165 plasmid. The clinical evolution has been monitored by angiography and estimated by walking time on the rolling carpet (Gardner protocol). Two months after therapy, all three patients showed complete relief of rest pain, improvement of ischaemic ulcer lesions and increased walking distance on the rolling carpet most probably due to appearance of newly formed collateral vessels.
Left ventricular (LV) free wall rupture is a potentially lethal mechanical complication after myocardial infarction (MI). Pericardial adhesions or slow extracardiac leak and pericardial inflammation may result in a contained cardiac rupture. LV pseudoaneurysm is a relatively uncommon clinical entity. It may occur after MI, but also as a complication of infective endocarditis, cardiac surgery, or trauma. Patients developing LV pseudoaneurysm after MI may present angina pectoris or signs of congestive heart failure (HF) but often are asymptomatic. Surgery is the treatment of choice for LV pseudoaneurysms diagnosed in the first months after MI. The management of chronic LV pseudoaneurysms is still subject of debate. This report highlights a 65-year-old patient newly hospitalized for acute decompensated HF who was diagnosed with a large chronic LV pseudoaneurysm and severe mitral regurgitation. The patient underwent successful resection of the pseudoaneurysm and patch repair of the ruptured ventricular wall. (ECHOCARDIOGRAPHY, Volume 25, November 2008) left ventricular pseudoaneurysm, mitral regurgitation, heart failure Left ventricular (LV) free wall rupture is a potentially lethal mechanical complication after myocardial infarction (MI). Pericardial adhesions or slow extracardiac leak and pericardial inflammation may result in a contained cardiac rupture. 1 LV pseudoaneurysm is a relatively uncommon clinical entity. It may occur after MI, but also as a complication of infective endocarditis, cardiac surgery, or trauma. Patients developing LV pseudoaneurysm after MI may present angina pectoris or signs of congestive heart failure (HF) but often are asymptomatic. 2 Surgery is the treatment of choice for LV pseudoaneurysms diagnosed in the first months after MI. 3-5 The management of chronic LV pseudoaneurysms is still a subject of debate. This report highlights a 65-year-old patient newly hospitalized for acute decompensated HF who was diagnosed with a large chronic LV pseudoaneurysm and severe mitral regurgitation.A 65-year-old female patient was admitted to our hospital for paroxysmal nocturnal dyspnea and severe fatigue. The patient presented exertional dyspnea for 6 months prior to admission and did not experience chest pain, palpitations or syncope. There was no history of cardiovascular disease and no significant cardiovascular risk factor. She was known to have calcified hydatid cyst of the liver. Physical examination revealed a regular heart rate of 100 beats/min, a blood pressure of 130/70 mmHg, a downward and leftward displacement of the apex, normal first and second heart sounds, a third heart sound, a grade 4/6 pansystolic murmur at the apex, and a grade 2/6 systolic murmur in the tricuspid valve area. Pulmonary auscultation showed bilateral crackles. The patient had tender hepatomegaly with systolic pulsations and bilateral pitting edema. Electrocardiogram showed sinus rhythm and a qR pattern in leads I and aVL. The posteroanterior chest x-ray showed global cardiomegaly and marked pulmonary venous con...
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