JOURNAL OF THE LOUISIANA STATE MEDICAL SOCIETY
usually falling in the distribution of a specific coronary artery found in coronary vasospasm. In addition, the diagnosis of Takotsubo cardiomyopathy appears to be less likely in patients with troponin T greater than 6ng/mL or troponin I greater than 15ng/mL, and its pattern doesn’t fall into the distribution of a single coronary artery. 4 In our case the patient had a troponin-T level of 19 ng/ml, and echocardiography didn't show any of the classic wall motion abnormalities usually described inTakotsubo cardiomyopathy. First described by Prinzmetal et al. in 1959, coronary arterial spasm is a reversible cause of myocardial ischemia commonly manifested by ST-segment elevation on the ECG. 5 By definition, it is a dynamic brief reduction in the luminal diameter of the epicardial coronary arteries attributed to an increase in vasomotor tone and eventually leading to myocardial ischemia. 6 The complete pathogenesis of coronary arterial spasm is not fully understood and includes a multifactorial process. The most acceptable hypotheses include the hyperactivity of coronary smooth muscle cells to constrictor stimuli (catecholamines, acetylcholine, and histamine), intrinsic endothelial dysfunction, and inappropriate regulation of alpha-adrenergic receptors of the autonomic nervous system. 7 Coronary arterial spasm more commonly affects younger patients and it is associated with other vasospastic conditions including migraine headaches and Raynaud’s phenomenon. 8 The incidence of coronary arterial spasm is decreasing secondary to medications that indirectly diminish it, especially calcium channel blockers. 7 Consequently, this rare condition is becoming less recognized and hence less considered in the differential diagnosis list of clinicians. 9
vasodilatory effects mediated by the increased production of nitric oxide. As a result, the incidence of vasospastic angina during pregnancy is unlikely. This may also explain the increased incidence of coronary arterial spasm in the postpartum period with the sudden drop of estrogen levels. 12 Oxytocinhormone has alsobeen identified as a potential inducer of peripartum coronary arterial spasm. Plasma levels of oxytocin rise significantly during labor. It is notable that exogenous oxytocin is occasionallyused in theperipartumperiod to increase uterine contraction. Oxytocin is a vasoactive peptide that causes relaxation of the smooth muscle decreasing arterial resistance and consequently leading to hypotension and tachycardia. In addition, this hormone has a vasocontrictive effect on coronary arteries. These concurrent mechanisms of oxytocin result in an oxygen supply and demand mismatch that can be manifested by chest pain, myocardial necrosis, and classic ischemic changes on the electrocardiogram. These ischemic manifestations are more pronounced in atherosclerotic coronary arteries, but can also be present in normal coronary vasculature. 13 " Coronary dissection accounts for up to 33% of myocardial infarctions in the postpartum period, and atherosclerotic diseasewith coronary thrombosis is the culprit in 21%. "
PATHOPHYSIOLOGY OF PERIPARTUM CORONARY VASOSPASM
DIAGNOSIS
Both experimental and clinical studies have shown that intra-coronary nitroglycerin administration can increase the angiographic cross-sectional area of normal coronary arteries by 30% to 50% of baseline. 14 Nitroglycerin not only augments myocardial oxygen supply by dilating epicardial coronary arteries and increasing subendocardial blood flow, but also diminishes myocardial oxygen demand by dilating both peripheral arteries and veins, leading to a decrease in left ventricular preload and afterload. 15 However, tolerance is a common and well-documented problem in animal models that is alsowidely accepted to be present in humans.16The diagnosis of coronary spasm is classically made angiographically by showing vasoconstriction that reverses with administration of nitroglycerin intravenously or directly to the coronary arteries. 8 Diagnosis can also be confirmed with the intracoronary injection of acetylcholine (Ach) to induce coronary arterial spasm, this, however, should be used with caution and reserved for only rare conditions, in view of the possible risk of severe intractable spasm leading to possible arrhythmia or death. The 2011 ACC/AHA guidelines had the provocation test as a class IIb recommendation in life-threatening cases with known anatomy. 17
Nitric oxide (NO); a vasodilator released by the endothelium, is an important regulator of coronary vascular tone. In endothelial dysfunction, there is commonly a deficiency in endothelium-mediated vasodilatation leading to coronary spasm at the injured segment. 10 Houck has suggested that endothelial dysfunction in the peripartum period is attributable to an immune-mediated process that can lead to postpartum dissection, thrombosis, or spasm. This abnormal immune response is activated by circulating fetal antigens that induce the production of antibodies against foreign antigens. These antibodies can cross-react with the coronary endothelium resulting in inflammation and impairing endothelial function. Consequently, patients with postpartum myocardial infarction may benefit from plasmapheresis treatment and intravenous immunoglobulin to suppress the antibody load. 11 In addition, both hormonal and hemodynamic changes present during pregnancy and the postpartum period have been suggested as causes of coronary arterial spasm. Authors have shown that estrogen has both short and long-term effects on the coronary vasculature. Estrogen has short-term coronary
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