| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
|
Interact CardioVasc Thorac Surg 2009;8:565-567. doi:10.1510/icvts.2008.189175 © 2009 European Association of Cardio-Thoracic Surgery
Acute ventricular rupture due to myocardial infarction during postpartum period k n Ender Topal*
Department of Cardiovascular Surgery, Dicle University Medicine Faculty, 21280 Diyarbak Received 24 July 2008; received in revised form 8 January 2009; accepted 8 January 2009
*Corresponding author. Tel.: +90-412-2488001; fax: +90-412-2488523.
Ventricular rupture is the third most common cause of deaths due to myocardial infarction. However, myocardial infarction is uncommon during pregnancy and postpartum period. We review a case with left ventricular rupture as a complication of myocardial infarction during postpartum period.
Key Words: Pregnancy; Myocardial infarction; Left ventricle; Rupture
Although acute myocardial infarction (MI) is a rare event in women of reproductive age (1/10,000 deliveries), pregnancy increases the risk three- to four-fold [1]. Physiological changes in pregnancy result in a procoagulant state and increasing stress on the cardiovascular system, particularly during delivery. Estradiol reduces the development of early lesions of atherosclerosis, in part through the effects on lipid metabolism which reduce lipid deposits in the endothelium. Once the atheroma is established, however, estrogens increase matrix metalloproteinases expression, which may promote disruption of the fibrous cap and subsequent rupture of the plaque. If the capsule does rupture causing turbulent blood flow, estradiol is thrombogenic and clot formation may occlude the arterial lumen [2]. Also, if myocardial infarction occurs within two weeks of labor or delivery, mortality may be as high as 45%.
A 43-year-old female presented to the emergency department with chest pain radiating through the left shoulder and arm. She also complained of dyspnea, sweating, weakness and headache. During pregnancy, she had been kept under control because of hypertension, but echocardiogram had been normal. Ten days earlier, subtotal hysterectomy was performed because of uterine rupture and fetal death of 7.5 months as a consequence of preeclampsia, two units of fresh blood was transfused and hypertension was controlled with methyldopa during hospitalization and later she was discharged on the third day. She was well until the last 30 h. Because of dyspnea and chest pain, she was observed for one day in two different local hospitals and sent to our hospital when she lost her consciousness. She was gravida 8, para 7. On physical examination, she was pale, apprehensive and clammy. Her blood pressure was too low to be measured. Her pulse was 130. The patient's temperature was 35 °C. On auscultation, heart sounds were heard deeply, lung sounds were bilaterally normal. Arterial blood gases on 5 l of oxygen were a pH of 7.426, PO2 of 71.6, PCO2 of 19.3 and HCO3 of 15.7. Biochemical analysis showed: white blood cell count 19.7 (raised neutrophils), hemoglobins 7.92, hematocrits 22.6, aspartate aminotransferase 317 U/l, alanine aminotransferase 107 U/l, lactate dehydrogenase 967 U/l, creatine kinase 362 U/l. Chest X-ray revealed an enlarged mediastinum and increased pulmonary vasculature. Widespread ST elevations and reciprocal ST depressions were seen in electrocardiography (ECG) (Fig. 1). (a) ST elevation in D2, D3, AVF, V2, V3, V4, V5 and V6 (>2 mm), (b) ST elevation in D1 (1 mm), (c) ST depression in AVR and V1.
In transthoracic echocardiogram (Fig. 2), lateral, posterior, anterior midapical walls were severely hypokinetic, ejection fraction was 35% and rupture of left ventricle apex was present.
As the patient's condition was urgent, we decided to repair the rupture firstly before coronary angiography. However, while the patient was being taken into the operating room, she arrested. Despite resuscitation and medical support, we were unable to keep the patient alive.
Although we could not encounter any case with ventricular rupture due to myocardial infarction during postpartum period or pregnancy in the literature; ECG changes, elevated cardiac enzymes, normal chamber sizes, hypokinetic myocardial walls and no history of trauma led us to believe that ‘the cause of the ventricular rupture was myocardial infarction’. For the most part, coronary heart disease during pregnancy or puerperium is preventable Cigarette smoking and overweight must be prohibited. For the women with diabetes, long-term control of glucose is needed to maintain a HbA1C level <7%. For hypercholesterolemia a healthy diet must be maintained, if not sufficient statins must be begun. Hypertension must be kept under control absolutely. Also exercise for half an hour a day is very beneficial [3]. Although in pregnancies with myocardial infarction in whom a post-mortem is carried out, coronary atherosclerosis is evident in 43% of subjects, spontaneous coronary artery dissection is the most common cause of myocardial infarction in the immediate postpartum period, no detectable evidence of coronary occlusion is found in around 75% of postpartum events [4]. In cases of coronary dissection, the etiology still remains unknown but may relate to changes in arterial histology, such as alteration in elastic and reticular fibers and muco-polysaccharide composition, which is a feature of normal gestation. This may be compounded by pre-existing risk factors for coronary heart disease including increasing blood volume/heart rate, myocardial oxygen requirements and anemia [5]. A susceptibility to coronary artery dissection in pregnancy may explain why hypertension is so strongly associated with acute myocardial infarction [6]. Hypertension may further damage blood vessels already weakened by hemodynamic stress or altered by other factors associated with pregnancy. The etiology of coronary artery disease in our patient was not identified because we did not have any time for coronary angiography and could not obtain permission to undergo post-mortem examination. However, we think that it might have been coronary dissection. This explains why she had no symptoms of coronary artery disease previously. Preeclampsia, particularly in association with preterm delivery, has been identified as a risk factor for myocardial infarction and mortality from cardiovascular disease later in life [7, 8]. Endothelial dysfunction persists in women with a history of preeclampsia for up to one year postpartum [9]. Hypertension, older age, multiparity, postpartum transfusion [4] and preeclampsia [7–10] were risk factors for MI in our patient. The highest incidence of acute myocardial infarction has been reported in multigravidas older than 33 years during the third trimester [10]. Women with an acute myocardial infarction are more likely to be multiparous than those without; however, parity is not associated with timing of acute myocardial infarction [5]. In most of the patients experiencing myocardial infarction during pregnancy, single-vessel disease, mainly left anterior descending artery, is observed [6] and their prognoses are not so serious. Nevertheless, the diagnosis of our patient was delayed and when she arrived at our hospital, it was too late to do anything. Early intervention to coronary artery (thrombolysis, coronary angioplasty or coronary bypass surgery) would have prevented ventricular rupture. Even after rupture, intra-aortic balloon support with pericardiocentesis might have saved her life. Rupture on the apex of left ventricle due to MI is seen rarely, contrary to our case. So it must be investigated whether there is any correlation between the site of ventricular rupture and pregnancy. Probably, pressure of the fetus and intra-abdominal organs to the heart, especially to apex, might play a role in formation of rupture. Permanent pressure to a local region may cause thinning of myocardium, and may also disrupt contraction and relaxation of muscles. Besides, pressure may cause endothelial dysfunction of coronary arteries and diminish blood flow to that region. Finally, all these factors may facilitate ventricular rupture afterwards, even when the fetus has already been taken out.
Coronary dissection may cause sudden death of a previously healthy woman during postpartum period. Therefore, the risk factors for myocardial infarction during pregnancy must be known and considered, especially preeclampsia.
Related Article
This article has been cited by other articles:
|
|||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |
Top
Abstract
1. Introduction
