Cardiovascular Diseases & Diagnosis

Segmental arterial mediolysis (SAM) is an uncommon arteriopathy that causes catastrophic abdominal hemorrhages, ischemic vascular changes and organ injury. Morphologic changes have suggested that SAM is a vasospastic disorder and that the responsible pressor agent is norepinephrine. This premise was strengthened by the finding of SAM in greyhound dogs administered ractopamine, a Beta-2 agonist capable or releasing norepinephrine from the peripheral sympathetic nervous system. This article will fortify this hypothesis by fitting the morphologic features and clinical presentations of SAM into events occurring in a stimulated peripheral sympathetic reflex arc. SAM is activated by non-physiological stimuli supplied by indirect acting sympathomimetic agonists. The stimulus is discrete usually limited to one vascular bed. A possible excessive quantity of norepinephrine is released which combines with hyper dense areas of alpha-1 adrenoceptors on the cell membranes of the medial smooth muscle. The alpha-1 adrenoceptor density is in a dynamic state influenced by a variety of exogenous and endogenous factors such as age, sex and prior exposure to sympathomimetic agonists all important components of SAM’s clinical presentation. There is a plasticity to these hyper dense areas accounting for the variable targeting of SAM in the stimulated arterial bed. The hyper dense zones of conformed alpha-1 adrenceptor intensely activates the smooth muscle intracellular Gq heterotrimeric protein setting into motion a perturbed cascade of biochemical events directed to causing vasoconstriction. These events create SAM’s pathology by 1) overloading the cytoplasm with Ca2+ causing mitochondrial dysfunction that terminates in mediolysis and/or apoptosis, 2) launching a powerful vasoconstrictive response that shears the outer media from the adventitia and 3) inaugurating an exaggerated reparative response that may angiographically resolve injurious arterial lesions or create sequelae including fibromuscular dysplasia. In conclusion evidence garnered from clinical and morphologic findings in SAM support the hypothesis that SAM represents a disorder of the peripheral sympathetic nervous system effectuated by a hyper density of the alpha-1 adrenoceptor.

Background: The purpose of this study was to assess epidemiological, clinical, and follow up data in a series of 15 patients consecutively admitted for Myocardial Infarction. Patients were black African and less than 45 years old. Methods: We conducted a retrospective study from January 1st 2010 to December 31st 2012 in the Yalgado Ouedraogo University Hospital in Burkina Faso. We assessed medical records of young patients less than 45 years of age who were consecutively admitted for Myocardial Infarction. Results: A total of 15 young subjects were admitted for myocardial infarction during the study period. Sex ratio was 2.75 for males; mean age was 35 ± 8 years with extremes of 21 and 45 years. Three main cardiovascular risk factors were noticed including hypertension (33.3%), diabetes and smoking (26.7%). Metabolic syndrome was found in three patients (20%). Revealing symptom of myocardial infarction was typical chest pain (80%) and ST + Acute Coronary Syndrome (ACS) diagnosed in all patients. 66.7% of patients were admitted more than 24 hours after the onset of their chest pain. EKG signs of necrosis were mostly found on anterior, septal, and lateral leads (26.7%). Doppler echocardiography found a systolic left ventricular dysfunction in 66.7% of cases. Thrombolysis was only used in 13.3% of patients. Complications were found in 86.7% of cases. Mortality rate was 20%. Conclusion: Myocardial infarction in young black African is more and more common in current cardiology practice. It is therefore necessary to adopt a proactive attitude, mostly primary prevention, targeting young people less than 45 years old.

Elderly are large sector of any community and they deserve our attention and care and this review article focus on the echocardiographic criteria in the elderly that may mimic or progress to cardiovascular disease.

We describe the case of a 9-year-old boy with uncorrected tetralogy of Fallot who presented with seizures at the computed tomography room during the preparation for cardiac computed tomography angiography in order to characterize the cardiac defect. The cardiac computed tomography angiography was suspended, and a brain computed tomography without contrast was performed followed by brain magnetic resonance imaging. The brain scan showed a large abscess in the right temporo-parietal region with important midline shift. The management of the patient was a combination of antibiotic therapy and osteoplastic craniotomy with removal of abscess capsule. At the discharge the patient looks well and no focal deficits on neurological examination were observed. Now-a-days he is following up with heart surgeons for correction of the tetralogy of Fallot. The aim of this report is highlight the importance of recognizing the brain abscess in patients with uncorrected congenital heart disease. The authors also discuss the better therapeutic option of this serious often fatal complication.