Post-partum myocardial ischemia due to intramuscular methylergonovine-induced coronary vasospasm: case report.

BACKGROUND: Methylergonovine is a vasoconstrictive agent historically used as a provocative agent in the lab for coronary vasospasm; it is also a first line uterotonic agent for management of postpartum hemorrhage. CASE PRESENTATION: A 29-year-old female with history of smoking and idiopathic thrombocytopenia received intramuscular methylergonovine after delivery of twins for intrauterine hemorrhage management. Subsequently, she had episodes of chest pain with high sensitivity Troponin I elevation to 1509 ng/L with accompanying septal T wave inversions, decreased left ventricular ejection fraction to 49% and basal septal wall hypokinesis. Computed tomography (CT) coronary angiogram showed patent coronary arteries and no coronary arterial dissection. The patient was conservatively managed with aspirin and metoprolol, and on follow up had fully recovered left ventricular function with resolution of wall motion abnormalities. Given this, coronary vasospasm due to intramuscular methylergonovine is the most likely cause of patient's chest pain and associated myocardial ischemia. CONCLUSIONS: Intramuscular, intrauterine, intravenous, and even oral methylergonovine can rarely cause coronary vasospasm leading to myocardial ischemia. Cardiologists caring for postpartum patients should be aware of these potential lethal complications; prompt identification and administration of sublingual nitroglycerin can prevent severe complications of arrythmias, heart block, or cardiac arrest.

Eclampsia with RCVS: Postpartum seizure provoked by methergine.

BACKGROUND: Eclampsia is a pregnancy complicationcharacterized bygeneralized tonic-clonicconvulsions.Not all seizures in pregnancy are eclamptic, and othercauses include epilepsy, infection,stroke,tumor, and ruptured aneurysm. CASE: A 19-year-old G1P0 presentedinlabor at term. She had a generalized tonic-clonicseizure one hour aftervaginaldelivery for which she received methergine for uterine atony. Seizure activity resolved with lorazepam and magnesium sulfate for presumed eclampsia.Brain imaging revealedvasoconstriction of theleftposterior cerebral artery and blood in the subarachnoid space,andshewas diagnosed with eclampsia with reversible cerebral vasoconstrictive syndrome (RCVS). CONCLUSION: RCVS isapregnancy-related cause of seizure that should remain on the differential for any patient presenting with a seizure in the peripartum period, especially with use of vasoconstrictive agents. Management is controversial but involves calcium channel blockers and magnesium sulfate, as well as avoidance of vasoconstrictive agents.

[A case of pulmonary alveolar hemorrhage caused by methylergometrine].

A 35-year-old woman underwent endometrial curettage for suspicion of miscarriage. A few minutes after intravenous injection of methylergometrin (0.2 mg) for inducing uterine contraction, blood gas analysis revealed severe hypoxemia. Chest CT showed diffuse ground-glass opacities in both lung fields and consolidation in the right lower lobe. Bronchoscopy revealed blood coagulation in the right bronchus intermedius. Bronchoalveolar lavage fluid showed fresh blood-like fluid containing hemosiderin-laden macrophages. We diagnosed pulmonary alveolar hemorrhage associated with pulmonary edema. Although we analyzed the possible causes of alveolar hemorrhage such as pulmonary thromboembolism, collagen disease, ANCA-related angitis and malignant disease, there were no underlying systemic diseases. It seems likely that contraction of the blood vessels caused by methylergometrin caused the increased pulmonary arterial and wedge pressure which led to pulmonary edema and alveolar hemorrhage. We believe this is the first reported case of pulmonary alveolar hemorrhage caused by methylergometrin, confirmed by bronchoscopy.

Postpartum myocardial infarction induced by methergine.

A 28-year-old woman presented to the emergency department for evaluation of acute chest pain. She lacked risk factors for coronary artery disease and her initial electrocardiogram (ECG) was nondiagnostic. Within 45 minutes of presentation she developed nausea, vomiting, restrosternal chest pain, and ECG changes compatible with an acute inferoposterior myocardial infarction. Emergent cardiac catheterization revealed three-vessel coronary artery ectasia and two-vessel occlusion. She underwent emergency coronary artery bypass grafting. Her myocardial ischemia was believed to have been induced by methergine, which she had been taking over the preceding 3 days. The etiology and pathophysiology of coronary artery ectasia, as well as the cardiovascular effects of methergine and a related drug, ergotamine, are discussed.

[A case of myocardial infarction associated with pulmonary edema during curettage for hydatidiform mole].

We experienced a case of myocardial infarction associated with pulmonary edema in a patient with hydatidiform mole probably due to methylergometrin and prostaglandin F2 alpha (PGF2 alpha) administered during the operation. A 26-year-old woman was scheduled to have curettage for hydatidiform mole under general anesthesia. She had no previous history of cardiopulmonary disease. During the operation, 0.4 mg of methylergometrin was administered intravenously to induce uterine contraction. Because the contraction was not sufficient, 2 mg of PGF2 alpha was given into the uterine muscle. A few minutes later blood pressure and heart rate increased abruptly and arterial blood gas analysis showed hypoxia and respiratory acidosis. Pulmonary edema was confirmed by chest X-P. After ordinary treatment for pulmonary edema, she was transferred to ICU. Postoperative examinations of ECG, serum enzymes and echocardiography revealed anterior subendocardial infarction. About one month later, methylergometrin test was performed during coronary angiography and this induced coronary vasospasm. PGF2 alpha is also known to cause peripheral as well as pulmonary vasoconstriction. Acute myocardial infarction induced by methylergometrin and PGF2 alpha may be a possible cause of this episode.

Cigarette smoking during coronary angiography: diffuse or focal narrowing (spasm) of the coronary arteries in 13 patients with angina at rest and normal coronary angiograms.

To evaluate the acute effects of cigarette smoking on coronary arteries (CA), repeated coronary angiograms were performed in 13 patients with angina at rest and with normal coronary angiograms at basal state, during smoking, and then after methylergometrine (MEM) and after intracoronary nitroglycerin. Smoking induced anginal pain in three patients, triggered spasm (focal narrowing) in six, and/or an abnormal segmental diffuse narrowing (greater than 30%) in eight. The narrowing of the left CA was on average -21 +/- 13% (P less than 0.001), with more important narrowing of the mid-left anterior descending (-29 +/- 19%, P less than 0.001). The mean of the maximal segmental narrowing by patient was -34 +/- 13% (P less than 0.001). MEM produced similar effects and induced focal CA spasms in nearly the same patients at the same sites. Cigarette smoking may induce vasoconstrictive effects on CA in patients with rest angina and normal coronary angiograms. This action is not dose-dependent and may be initiated by less than one cigarette. These observations offer a new perspective for the understanding of the role of smoking in the precipitation of coronary events.