CLINICAL OBSTETRICS AND GYNECOLOGY Volume 57, Number 4, 835–843 r 2014, Lippincott Williams & Wilkins
Acute Myocardial Infarction During Pregnancy LUIS D. PACHECO, MD,*w GEORGE R. SAADE, MD,* and GARY D.V. HANKINS, MD* *Department of Obstetrics & Gynecology, Division of Maternal-Fetal Medicine; and w Department of Anesthesiology, Division of Surgical Critical Care, The University of Texas Medical Branch at Galveston, Galveston, Texas Abstract: Myocardial infarction complicating pregnancy is an important cause of maternal morbidity and mortality. The coexistence of obesity, diabetes, chronic hypertension, and delayed age at pregnancy is expected to increase the prevalence of myocardial infarction during pregnancy. Timely treatment in the form of percutaneous coronary intervention has dramatically improved outcomes. Early medical treatment with antiplatelet and antithrombotic agents is important, and maternal fetal medicine specialists must be familiar with it. In this article we will describe the basic initial medical management of patients with an acute coronary syndrome. Key words: pregnancy, myocardial infarction, coronary artery disease
Introduction Acute myocardial infarction (MI) may occur during pregnancy and lead to significant morbidity and mortality to both the mother and the fetus. The additive effects of women postponing pregnancy until more advanced ages, the obesity epidemic, and a higher Correspondence: Luis D. Pacheco, MD, The University of Texas Medical Branch at Galveston, 301 University Blvd., Galveston, TX. E-mail: [email protected] The authors declare that they have nothing to disclose. CLINICAL OBSTETRICS AND GYNECOLOGY
/
prevalence of chronic hypertension and diabetes (as a result of more advanced maternal age and higher body mass index) makes MI a more common condition during pregnancy compared with decades ago. The 2 most common causes of maternal deaths from cardiac origin include aortic dissection and MI.1 Furthermore, the risk of MI is increased by a factor of 3 to 4 during pregnancy and postpartum compared with age-matched nonpregnant individuals.2 The latter is likely explained by the hypercoagulable state of pregnancy. The most common cause of MI is rupture of an atherosclerotic plaque with platelet aggregation leading to acute coronary occlusion. Partial occlusion leads to a nonelevated ST segment MI, whereas complete occlusion causes a ST segment elevation MI. Nonatherosclerotic causes of MI are listed in Table 1. CLINICAL PRESENTATION AND DIAGNOSIS
The symptoms of MI are more intense than those of angina and usually last for VOLUME 57
/
NUMBER 4
/
DECEMBER 2014
www.clinicalobgyn.com | 835
836
Pacheco et al
TABLE 1.
Nonatherosclerotic Causes of Myocardial Infarction
Arteritis (Kawasaki, Takayasu, polyarteritis nodosa, collagen diseases) Coronary vasospasm (Prinzmetal angina, cocaine abuse) Coronary dissection (peripartum period) Stress cardiomyopathy (Takotsubo cardiomyopathy) Embolism from left heart cavities thrombi or endocarditis In situ thrombosis from congenital or acquired thrombophilias Aortic dissection extending into the coronary arteries
periods of 15 to 20 minutes. Usually patients complain of chest pain or pressure (that may or may not radiate to the jaw, neck, or arms), shortness of breath, nausea/vomiting, diaphoresis, and dizziness. Severe cases in which a large portion of the myocardium is compromised may manifest with hypotension due to decreased cardiac output and cardiogenic pulmonary edema (cardiogenic shock). Atypical symptoms (sharp chest pain, painless MI, indigestion, or epigastric pain) are more common among women and patients with diabetes. The suspected clinical diagnosis is usually confirmed with electrocardiographic changes and elevation of markers of myocardial necrosis. The electrocardiogram (EKG) will classify patients into 2 main groups: ST segment elevation MI and non-ST segment elevation MI. This distinction is fundamental in deciding treatment strategies as will be discussed later. Non-ST MI will usually have ST segment depression or T-wave inversions in Z2 contiguous leads but may present with minimal changes on the EKG or even a normal initial EKG. Typically, these patients will have a partial occlusion of the vessel. ST segment elevation MI will usually show elevation of the ST segment in Z2 contiguous leads, a new or indeterminate left bundle block, or ST depression in the right-sided precordial leads (V1 through www.clinicalobgyn.com
V4), indicating a posterior wall MI. Any of the latter 3 situations will classify the event as an ST MI. Patients with ST MIs usually have a complete vessel occlusion.1 A normal EKG does not rule out a coronary event, as up to 18% of patients with a documented MI may present initially with a normal EKG. Cardiac troponins (I and T) are the most sensitive and specific markers of myocardial necrosis.3 Troponin elevation indicates myocardial necrosis. Certain other conditions may also elevate troponins and not necessarily secondary to coronary artery disease. Both myocarditis and pericarditis may lead to troponin leakage. Cytokines may injure the myocardium with concomitant troponin elevations in the setting of sepsis.4 Pressure elevations inside the ventricles, such as increased right ventricular pressure in the setting of an acute pulmonary embolism or acute elevations in the left ventricular pressures in cases of hypertensive emergencies may compress small subendocardial vessels with diffuse ischemia and troponin leakage.5 Troponins are detected in serum within 4 to 6 hours of symptom onset. Importantly, levels may be undetectable soon after an MI, and negative values should not be used to rule out the diagnosis if clinical suspicion is high. Once elevated, troponins will remain elevated for 1 to 2 weeks. This period may be even more prolonged in patients with renal dysfunction, as the kidney clears troponins.6 Levels of troponins are not elevated during normal pregnancy, and any elevation should be considered abnormal. In summary, the diagnosis of a MI is based on clinical presentation and supported by changes in the EKG and evidence of myocardial necrosis as reflected by elevated troponins in serum. TREATMENT OF A NON-ST MI
Basic initial treatment includes assuring the presence of a patent airway and
Acute Myocardial Infarction During Pregnancy maintaining both hemodynamic and rhythm stability. Oxygen administration is routine. Persistent chest pain may be treated with sublingual nitroglycerin, morphine sulfate, or intravenous nitroglycerine. The use of nitroglycerine is contraindicated in cases of a right ventricular infarct, as this agent’s ability to cause significant venodilation may compromise preload. Nitroglycerin dilates the coronary arteries and decreases preload and afterload with subsequent decrease in oxygen consumption. If sublingual nitroglycerin is ineffective, intravenous administration may be considered. Morphine sulfate decreases pain and anxiety and also leads to venodilation with less preload. Recent data have raised questions about the safety of morphine in the setting of a non-ST MI due to hypotension associated with its use, and morphine’s use in patients with a non-ST MI has been downgraded to a class IIa recommendation.7 Tachycardia and hypertension should be addressed and treated as needed with b-blockers or calcium channel blockers.8 Metoprolol, atenolol, or esmolol may be utilized. In patients with persistent chest pain, tachycardia, or hypertension, the intravenous route may be preferred. In the absence of these symptoms, the oral route is preferred. In patients with low systolic blood pressures (eg, 110/min), the possibility that the tachycardia is compensatory to maintain an adequate cardiac output must be entertained. Ideally, an echocardiography should be done before b-blockade in this population to avoid precipitation of cardiogenic shock if the ventricular contractility is severely compromised. b-blockers should be avoided in patients with severe asthma or chronic obstructive pulmonary disease, pulmonary edema from left ventricular failure, systolic blood pressure
Acute Myocardial Infarction During Pregnancy LUIS D. PACHECO, MD,*w GEORGE R. SAADE, MD,* and GARY D.V. HANKINS, MD* *Department of Obstetrics & Gynecology, Division of Maternal-Fetal Medicine; and w Department of Anesthesiology, Division of Surgical Critical Care, The University of Texas Medical Branch at Galveston, Galveston, Texas Abstract: Myocardial infarction complicating pregnancy is an important cause of maternal morbidity and mortality. The coexistence of obesity, diabetes, chronic hypertension, and delayed age at pregnancy is expected to increase the prevalence of myocardial infarction during pregnancy. Timely treatment in the form of percutaneous coronary intervention has dramatically improved outcomes. Early medical treatment with antiplatelet and antithrombotic agents is important, and maternal fetal medicine specialists must be familiar with it. In this article we will describe the basic initial medical management of patients with an acute coronary syndrome. Key words: pregnancy, myocardial infarction, coronary artery disease
Introduction Acute myocardial infarction (MI) may occur during pregnancy and lead to significant morbidity and mortality to both the mother and the fetus. The additive effects of women postponing pregnancy until more advanced ages, the obesity epidemic, and a higher Correspondence: Luis D. Pacheco, MD, The University of Texas Medical Branch at Galveston, 301 University Blvd., Galveston, TX. E-mail: [email protected] The authors declare that they have nothing to disclose. CLINICAL OBSTETRICS AND GYNECOLOGY
/
prevalence of chronic hypertension and diabetes (as a result of more advanced maternal age and higher body mass index) makes MI a more common condition during pregnancy compared with decades ago. The 2 most common causes of maternal deaths from cardiac origin include aortic dissection and MI.1 Furthermore, the risk of MI is increased by a factor of 3 to 4 during pregnancy and postpartum compared with age-matched nonpregnant individuals.2 The latter is likely explained by the hypercoagulable state of pregnancy. The most common cause of MI is rupture of an atherosclerotic plaque with platelet aggregation leading to acute coronary occlusion. Partial occlusion leads to a nonelevated ST segment MI, whereas complete occlusion causes a ST segment elevation MI. Nonatherosclerotic causes of MI are listed in Table 1. CLINICAL PRESENTATION AND DIAGNOSIS
The symptoms of MI are more intense than those of angina and usually last for VOLUME 57
/
NUMBER 4
/
DECEMBER 2014
www.clinicalobgyn.com | 835
836
Pacheco et al
TABLE 1.
Nonatherosclerotic Causes of Myocardial Infarction
Arteritis (Kawasaki, Takayasu, polyarteritis nodosa, collagen diseases) Coronary vasospasm (Prinzmetal angina, cocaine abuse) Coronary dissection (peripartum period) Stress cardiomyopathy (Takotsubo cardiomyopathy) Embolism from left heart cavities thrombi or endocarditis In situ thrombosis from congenital or acquired thrombophilias Aortic dissection extending into the coronary arteries
periods of 15 to 20 minutes. Usually patients complain of chest pain or pressure (that may or may not radiate to the jaw, neck, or arms), shortness of breath, nausea/vomiting, diaphoresis, and dizziness. Severe cases in which a large portion of the myocardium is compromised may manifest with hypotension due to decreased cardiac output and cardiogenic pulmonary edema (cardiogenic shock). Atypical symptoms (sharp chest pain, painless MI, indigestion, or epigastric pain) are more common among women and patients with diabetes. The suspected clinical diagnosis is usually confirmed with electrocardiographic changes and elevation of markers of myocardial necrosis. The electrocardiogram (EKG) will classify patients into 2 main groups: ST segment elevation MI and non-ST segment elevation MI. This distinction is fundamental in deciding treatment strategies as will be discussed later. Non-ST MI will usually have ST segment depression or T-wave inversions in Z2 contiguous leads but may present with minimal changes on the EKG or even a normal initial EKG. Typically, these patients will have a partial occlusion of the vessel. ST segment elevation MI will usually show elevation of the ST segment in Z2 contiguous leads, a new or indeterminate left bundle block, or ST depression in the right-sided precordial leads (V1 through www.clinicalobgyn.com
V4), indicating a posterior wall MI. Any of the latter 3 situations will classify the event as an ST MI. Patients with ST MIs usually have a complete vessel occlusion.1 A normal EKG does not rule out a coronary event, as up to 18% of patients with a documented MI may present initially with a normal EKG. Cardiac troponins (I and T) are the most sensitive and specific markers of myocardial necrosis.3 Troponin elevation indicates myocardial necrosis. Certain other conditions may also elevate troponins and not necessarily secondary to coronary artery disease. Both myocarditis and pericarditis may lead to troponin leakage. Cytokines may injure the myocardium with concomitant troponin elevations in the setting of sepsis.4 Pressure elevations inside the ventricles, such as increased right ventricular pressure in the setting of an acute pulmonary embolism or acute elevations in the left ventricular pressures in cases of hypertensive emergencies may compress small subendocardial vessels with diffuse ischemia and troponin leakage.5 Troponins are detected in serum within 4 to 6 hours of symptom onset. Importantly, levels may be undetectable soon after an MI, and negative values should not be used to rule out the diagnosis if clinical suspicion is high. Once elevated, troponins will remain elevated for 1 to 2 weeks. This period may be even more prolonged in patients with renal dysfunction, as the kidney clears troponins.6 Levels of troponins are not elevated during normal pregnancy, and any elevation should be considered abnormal. In summary, the diagnosis of a MI is based on clinical presentation and supported by changes in the EKG and evidence of myocardial necrosis as reflected by elevated troponins in serum. TREATMENT OF A NON-ST MI
Basic initial treatment includes assuring the presence of a patent airway and
Acute Myocardial Infarction During Pregnancy maintaining both hemodynamic and rhythm stability. Oxygen administration is routine. Persistent chest pain may be treated with sublingual nitroglycerin, morphine sulfate, or intravenous nitroglycerine. The use of nitroglycerine is contraindicated in cases of a right ventricular infarct, as this agent’s ability to cause significant venodilation may compromise preload. Nitroglycerin dilates the coronary arteries and decreases preload and afterload with subsequent decrease in oxygen consumption. If sublingual nitroglycerin is ineffective, intravenous administration may be considered. Morphine sulfate decreases pain and anxiety and also leads to venodilation with less preload. Recent data have raised questions about the safety of morphine in the setting of a non-ST MI due to hypotension associated with its use, and morphine’s use in patients with a non-ST MI has been downgraded to a class IIa recommendation.7 Tachycardia and hypertension should be addressed and treated as needed with b-blockers or calcium channel blockers.8 Metoprolol, atenolol, or esmolol may be utilized. In patients with persistent chest pain, tachycardia, or hypertension, the intravenous route may be preferred. In the absence of these symptoms, the oral route is preferred. In patients with low systolic blood pressures (eg, 110/min), the possibility that the tachycardia is compensatory to maintain an adequate cardiac output must be entertained. Ideally, an echocardiography should be done before b-blockade in this population to avoid precipitation of cardiogenic shock if the ventricular contractility is severely compromised. b-blockers should be avoided in patients with severe asthma or chronic obstructive pulmonary disease, pulmonary edema from left ventricular failure, systolic blood pressure
