Summary:The vast majority of left ventricular aneurysms (LVA) are secondary to coronary artery disease. The natural history of LVA is now better understood. The increasing use of noninvasive techniques has allowed earlier recognition and better appreciation of LVA genesis and pathophysiology . Improvements in surgical anesthesia and techniques have resulted in more successful LVA surgery. This article reviews the pathogenesis, natural history, and complications of LVA. Surgical indications and available treatment options in the management of patients with LVA and severe symptoms are presented. Left ventricular pseudoaneurysm (false aneurysm) will also be discussed.Key words: noninvasive techniques, ventricular amhythmias, congestive heart failure, endocardial resection, left ventricular aneurysmectomy DefinitionsThe marked variability in the definition of LVA is partly responsible for difficulties encountered in studying different reports regarding the natural history and treatment of the entity. Definitions vary across different disciplines and technologies. To the pathologist, LVA usually refers to a thin and stretched area of the ventricle where mature scar tissue has replaced most of the myocardium. T o the physiologist and clinician, LVA is best defined as a portion of the ventricle that manifests systolic expansion ir- respective of histologic structure. The surgeon's definition essentially agrees with the pathologist's.For the purpose of this discussion, LVA is defined as a localized protrusion of the left ventricular (LV) cavity during systole and diastole with akinetic or dyskinetic walls. EtiologyLeft ventricular aneurysm most commonly results from acute myocardial infarction (MI). An incidence varying from 3.5 to 5% has been reported in autopsy studies.',2 Angiographically defined LVA has been reported in 7.6% of patients with coronary arteIy disease referred for coronary angi~graphy.~ On the other hand, in selected patients undergoing radionuclide angiography soon after MI, 35 % had LVA.4 Greater than 80% of left ventricular aneurysms involve the anterior wall and/or apex and are associated with high-grade stenosis or complete occlusion of the proximal or mid-left anterior descending coronary artery (LAD).3-5 The presence of only three muscle layers at the apex (compared with four layers at the base) explains the predeliction of the apex to LVA formation. Myocardial infarction is usually transmural and is associated with high peak levels of the enzyme creatine k i n a~e .~.~ Approximately 50% of left ventricular aneurysms occumng after acute MI appear within 48 h from the onset of chest pain. The remainder appear within two weeks.4 Once formed, LVA rarely resolves. Myocardial infarction and LVA may result from coronary arterial emboli or anomalous origin of the left coronary artery from the pulmonary artery.Not all patients with coronary atherosclerosis have scar tissue in the area of LVA. Transient occlusion of a coronary artery may result in reversible dyskinesis (physiologic LVA).' Patients with i...

No abstract

Migraine is a chronic disease with episodic attacks, which, when frequent or severe, can be associated with poor quality of life, increased health resource utilization, lost productivity, and significant disability. Preventive therapy can therefore have a significant beneficial clinical and economic impact. However, many migraineurs are treated suboptimally. There is increasing evidence that activation and degranulation of meningeal mast cells result in meningeal irritation, vascular dilation, and stimulation of nearby nociceptive nerve endings of the trigeminal nerve, thus potentially contributing to the pathogenesis of migraine headache. The renin angiotensin system and its peptides are well represented in the mammalian central nervous system and can also promote neurogenic inflammation. Interestingly, mast cells are capable of releasing renin and increasing local production of Angiotensin II. We therefore hypothesize that mast cells contribute to migraine headache through activation of the renin angiotensin system. This hypothesis may help explain the association between migraine and cardiovascular disease as well as observations that medications that modulate the renin angiotensin system can reduce migraine-related morbidity in patients with frequently recurring migraine attacks.