Coronary Artery Aneurysms: Comprehensive Review and a Case Report of a Left Main Coronary Artery Aneurysm.

Coronary artery aneurysms (CAAs) are rare anatomical disorders of the coronary arteries. Atherosclerosis and Kawasaki disease are the principal causes of CCAs, while other causes including genetic factors, inflammatory arterial diseases, connective tissue disorders, endothelial damage after cocaine use, iatrogenic complications after interventions and infections, are also common among patients with CAAs. Although there is a variety of noninvasive methods including echocardiography, computed tomography, and magnetic resonance imaging, coronary angiography remains the gold standard diagnostic method. There is still no consensus about the most appropriate therapeutic strategy. Medical therapy including antiplatelets, anticoagulants, statins and ACEs are preferred either in patients with atherosclerosis, inflammatory status and stable CAAs, while percutaneous or surgery interventions are usually applied in patients with acute coronary syndrome due to a CAA culprit, obstructive coronary artery disease or large saccular aneurysms at a high risk of rupturing.

Spontaneous coronary artery dissection: A review of diagnostic methods and management strategies.

Spontaneous coronary artery dissection (SCAD) is a rare non-atherosclerotic cause of acute coronary syndromes defined as non-iatrogenic, non-traumatic separation of the coronary artery wall. The most common profile is a middle-aged woman between 44 and 53 years with few cardiovascular risk factors. SCAD is frequently linked with predisposing factors, such as postpartum, fibromuscular dysplasia or other vasculopathies, connective tissue disease and hormonal therapy, and it is often triggered by intense physical or emotional stress, sympathomimetic drugs, childbirth and activities increasing shear stress of the coronary artery walls. Patients with SCAD usually present at the emergency department with chest discomfort, chest pain, and rapid heartbeat or fluttery. During the last decades, the most common problem of SCAD was the lack of awareness about this condition which has led to significant underdiagnosis and misdiagnosis. However, modern imaging techniques such as optical coherence tomography, intravascular ultrasound, coronary angiography or magnetic resonance imaging have contributed to the early diagnosis of the disease. Treatment of SCAD remains controversial, especially during the last years, where invasive techniques are being used more often and in more emergent cardiac syndromes. Although conservative treatment combining aspirin and beta-blocker remains the recommended strategy in most cases, revascularization could also be suggested as a method of treatment in specific indications, but with a higher risk of complications. The prognosis of SCAD is usually good and long-term mortality seems to be low in these patients. Follow-up should be performed on a regular basis.

Prevalence of heterozygous familial hypercholesterolemia and combined hyperlipidemia phenotype in very young survivors of myocardial infarction and their association with the severity of atheromatous burden.

BACKGROUND: Heterozygous familial hypercholesterolemia (HeFH) and combined hyperlipidemia (CHL) phenotype are associated with premature myocardial infarction (MI). OBJECTIVE: To assess the prevalence of HeFH and CHL phenotype among young survivors of MI and compare patients' characteristics with these 2 lipid disorders. METHODS: We recruited 382 young survivors of MI (≤40 years). Fasting lipids, lipoprotein(a) [Lp(a)], apolipoprotein A-1, and apolipoprotein B (apoB) levels were determined. Using the Dutch Lipid Clinic Network (DLCN) algorithm, patients having definite or probable HeFH were identified. Patients with apoB levels >120 mg/dL and triglyceride levels >170 mg/dL (1.92 mmol/L) [>90th percentile of 326 age and sex-matched healthy controls] were classified as having CHL phenotype. Common carotid artery intima-media thickness (CCA-IMT) was measured by B-mode ultrasonography. RESULTS: Eighty-one patients (21.2%) had definite/probable HeFH and 62 (16.2%) had CHL phenotype. Twenty-three patients fulfilled the criteria for both HeFH and CHL phenotype and were removed from further comparisons. Patients with HeFH (n = 58) had higher levels of total cholesterol, low-density lipoprotein (LDL)-cholesterol, Lp(a), and apoB, whereas patients with CHL phenotype (n = 39) had higher levels of triglycerides and lower high-density lipoprotein (HDL)-cholesterol levels. The prevalence of metabolic syndrome was higher in patients with CHL phenotype compared to those with HeFH (67.0% vs 16.4%, P < .001). Patients with HeFH had more extensive coronary artery disease (3-vessel disease: 36.2% vs 12.8%, P = .011) and greater right CCA-IMT (0.67 ± 0.11 mm vs 0.56 ± 0.09 mm, P < .001) and left CCA-IMT (0.68 ± 0.10 mm vs 0.56 ± 0.08 mm, P < .001) compared to CHL phenotype patients. CONCLUSIONS: Both HeFH and CHL phenotype are common among patients with premature MI. CHL phenotype compared to HeFH is associated with less atheromatous burden in coronary and carotid arteries at the time of first MI.