Complete Angiographic Resolution of Cocaine Induced Coronary Artery Dissection within Eight Days without Coronary Stenting--A Case Report.

INTRODUCTION: Coronary dissection is a rarely reported complication of cocaine use for which there are no specific guidelines on management despite the widespread use of the drug. METHODS: We report a case of a 26-year-old otherwise fit and healthy Caucasian male smoker who presented to our facility with an infero-lateral ST elevation myocardial infarction (STEMI) following nasal inhalation of 1 gram of cocaine. Coronary angiography showed a mid left anterior descending (LAD) artery dissection with distal occlusive embolism and another dissection of the distal right coronary artery (RCA) with embolism and occlusion of the distal posterolateral branch. OUTCOME: Wiring of both vessels with a High-Torque Floppy wire successfully re-established TIMI 3 flow with relief of pain and resolution of his ST-segment elevation. Given the absence of any flow-limiting lesions, stenting was avoided. He was subsequently put on a combination of therapeutic dose enoxaparin, aspirin, ticagrelor, atorvastatin and metoprolol. A repeat angiogram eight days later showed complete healing of the dissections. CONCLUSION: This case shows that percutaneous management without stenting coupled with aggressive anti-coagulation of cocaine induced coronary dissection may result in an acceptable outcome especially in a young otherwise fit and healthy patient.

Corticosteroids and Spontaneous Coronary Artery Dissection: A New Predisposing Factor?

We describe the case of a 39-year-old woman with spontaneous coronary artery dissection (SCAD) of the left circumflex artery. We postulate that her SCAD was precipitated by high-dose corticosteroid use for the treatment of optic neuritis. The epidemiology and known risk factors of SCAD are reviewed with an additional focus on the effect of corticosteroids on the cardiovascular system.

Cocaine-induced postpartum coronary artery dissection: a case report and 80-year review of literature.

The incidence of cocaine-induced myocardial infarction (MI) in pregnancy is unknown. During the peripartum period, cocaine-abusing women are highly susceptible to MI caused by the effect of cocaine on a heart that is already stressed by hemodynamic changes of pregnancy. MI is an infrequent event during pregnancy and the peripartum period, with an estimated rate of 1 in 16,000 patients. Spontaneous coronary artery dissection (SCAD) can account for up to 27% of pregnancy-related MIs. We describe a case of MI diagnosed by increased troponin I levels in a postpartum patient with recent crack cocaine use in the setting of SCAD that required percutaneous coronary intervention of the left anterior descending and diagonal arteries. We also provide a comprehensive review of published literature related to this clinical entity.

Developmental defects of coronary vasculature in rat embryos administered bis-diamine.

BACKGROUND: Conotruncal anomalies are often associated with abnormal coronary arteries. Although bis-diamine is known to induce conotruncal defects, its pathological effects on coronary vascular development have not been demonstrated. This study sought to assess the teratogenic effects of bis-diamine on coronary vascular development and the pathogenesis of this anomalous association. METHODS AND RESULTS: A single 200 mg dose of bis-diamine was administered to pregnant Wistar rats at 10.5 days of gestation. Fifty-two embryos from 10 mother rats underwent morphological analysis of the coronary arteries. Three embryos each were removed from four mothers on embryonic days (ED) 14.5, 15.5, 16.5, and 17.5 and used for immunohistochemical studies using the anti-vascular cell adhesion molecule (VCAM)-1 antibody. Conotruncal anomalies were detected in 48 of 52 embryos, and an aplastic or hypoplastic left coronary artery was found in all of them. In control embryos at ED 16.5, VCAM-1-positive epicardial cells were transformed into mesenchymal cells in vascular plexus, which appeared to differentiate into the endothelial cells of coronary vasculature. In the heart at ED 17.5, coronary vasculature was well developed and connected with coronary ostia near the aorta. However, poor epicardial-mesenchymal transformation and subsequent differentiation was revealed in bis-diamine-treated embryos at EDs 16.5 and 17.5, causing abnormal development of the coronary vasculature and incomplete connections with coronary ostia of the aorta. CONCLUSIONS: Anomalous coronary arteries in the bis-diamine-treated embryos are induced by the disruption of epicardial-mesenchymal transformation and subsequent poor development of coronary vasculature. Incomplete hatching of the coronary ostium is associated with abnormal truncal division.

Juvenile exposure to anthracyclines impairs cardiac progenitor cell function and vascularization resulting in greater susceptibility to stress-induced myocardial injury in adult mice.

BACKGROUND: The anthracycline doxorubicin is an effective chemotherapeutic agent used to treat pediatric cancers but is associated with cardiotoxicity that can manifest many years after the initial exposure. To date, very little is known about the mechanism of this late-onset cardiotoxicity. METHODS AND RESULTS: To understand this problem, we developed a pediatric model of late-onset doxorubicin-induced cardiotoxicity in which juvenile mice were exposed to doxorubicin, using a cumulative dose that did not induce acute cardiotoxicity. These mice developed normally and had no obvious cardiac abnormalities as adults. However, evaluation of the vasculature revealed that juvenile doxorubicin exposure impaired vascular development, resulting in abnormal vascular architecture in the hearts with less branching and decreased capillary density. Both physiological and pathological stress induced late-onset cardiotoxicity in the adult doxorubicin-treated mice. Moreover, adult mice subjected to myocardial infarction developed rapid heart failure, which correlated with a failure to increase capillary density in the injured area. Progenitor cells participate in regeneration and blood vessel formation after a myocardial infarction, but doxorubicin-treated mice had fewer progenitor cells in the infarct border zone. Interestingly, doxorubicin treatment reduced proliferation and differentiation of the progenitor cells into cells of cardiac lineages. CONCLUSIONS: Our data suggest that anthracycline treatment impairs vascular development as well as progenitor cell function in the young heart, resulting in an adult heart that is more susceptible to stress.

Angioarchitecture of the venous and capillary system in heart defects induced by retinoic acid in mice.

BACKGROUND: Corrosion casting and immunohistochemical staining with anti-alpha smooth muscle actin and anti-CD34 was utilized to demonstrate the capillary plexus and venous system in control and malformed mouse hearts. METHODS: Outflow tract malformations (e.g., double outlet right ventricle, transposition of the great arteries, and common truncus arteriosus) were induced in progeny of pregnant mice by retinoic acid administration at day 8.5 of pregnancy. RESULTS: Although control hearts exhibited areas in which capillaries tended to be oriented in parallel arrays, the orientation of capillaries in the respective areas of malformed hearts was chaotic and disorganized. The major branch of a conal vein in control hearts runs usually from the left side of the conus to its right side at the root of the pulmonary trunk and opens to the right atrium below the right auricle; thus, it has a curved course. On the other hand, a conal vein in malformed hearts courses from the left side or from the anterior side of the conus and tends to traverse straight upwards along the dextroposed aorta or along the aortopulmonary groove with its proximal part located outside of the heart. Other cardiac veins in outflow tract malformations are positioned in the same locations as in control hearts. CONCLUSIONS: We postulate that the changed location of the conal vein and disorganized capillary plexus result from malformed morphogenesis of the outflow tract and/or a disturbed regulation of angiogenic growth factor release from the adjacent environment.

Coronary artery embryogenesis in cardiac defects induced by retinoic acid in mice.

BACKGROUND: Although normal coronary artery embryogenesis is well described in the literature, little is known about the development of coronary vessels in abnormal hearts. METHODS: We used an animal model of retinoic acid (RA)-evoked outflow tract malformations (e.g., double outlet right ventricle [DORV], transposition of the great arteries [TGA], and common truncus arteriosus [CTA]) to study the embryogenesis of coronary arteries using endothelial cell markers (anti-PECAM-1 antibodies and Griffonia simplicifolia I (GSI) lectin). These markers were applied to serial sections of staged mouse hearts to demonstrate the location of coronary artery primordia. RESULTS: In malformations with a dextropositioned aorta, the shape of the peritruncal plexus, from which the coronary arteries develop, differed from that of control hearts. This difference in the shape of the early capillary plexus in the control and RA-treated hearts depends on the position of the aorta relative to the pulmonary trunk. In both normal and RA-treated hearts, there are several capillary penetrations to each aortic sinus facing the pulmonary trunk, but eventually only 1 coronary artery establishes patency with 1 aortic sinus. CONCLUSIONS: The abnormal location of the vessel primordia induces defective courses of coronary arteries; creates fistulas, a single coronary artery, and dilated vessel lumens; and leaves certain areas of the heart devoid of coronary artery branches. RA-evoked heart malformations may be a useful model for elucidating abnormal patterns of coronary artery development and may shed some light on the angiogenesis of coronary artery formation.

Cardiovascular malformations experimentally induced in the rat.

Sprague-Dawley rats were treated with glycerol formal during days 6-15 of gestation. 76 to 193 fetuses of these rats examined for visceral malformations showed abnormalities of the heart and great vessels. The principal cardiac malformation was ventricular septum defect associated in 40% of the cases with anomalies of the aortic arch: double aortic arch, right aortic arch and coarctation of the aorta. An attempt was made to explain the specific cardiovascular defects.