The session discusses the imaging in pregnancy through a case-based approach. It also focuses on the physiology of normal pregnancy and the implications for cardiac imaging, imaging modalities and peripartum cardiomyopathy and evolving imaging markers of CVD risk conferred by pregnancy associated conditions.

The first case, a 35 year old with 5 prior pregnancies, no deliveries, no live births presents for induction of labor at 40 weeks. She had mild orthopnea 2 weeks prior to delivery. She underwent a C-section due to a non-reassuring fetal heart tracing and arrest of dilation. One hour post-surgery she developed shortness of breath with hypoxia up to 10L O2. She had a history of dilated cardiomyopathy, polycystic ovarian disease and depression/anxiety. She had mild pleural effusion. A transthoracic echocardiogram (TE) revealed mitral severe regurgitation. She was administered IV Lasix to which there was an excellent response and improvement for hypoxia. There was a complete resolution and improvement in her volume status after a few days. The diagnosis was thought to be hypoxia secondary to pulmonary edema in the setting of a newly discovered severe mitral regurgitation and a mildly dilated LV. A repeat TE after 6 weeks later showed marked improvement in her mitral regurgitation. The learning points from this case are that valvular, regurgitant lesions in pregnancy are generally well- tolerated. With moderate to severe lesions, symptomatic volume overload can occur in the 2nd and 3rd trimester and, particularly in the 24 to 32 hours post-delivery as cardiac output peaks. There are significant volume shifts and volume status which can be managed successfully with diuretics and some after load reduction.

The 2nd case was a 36 year old G2P1011 woman with recent in vitro fertilization and uncomplicated pregnancy after a spontaneous vaginal delivery presenting with postpartum day 4 with sudden onset chest pain. On arrival at the emergency department, the patient appeared normal, no murmurs or pronounced cardiac sounds and heart rate 40-60 beats per minute. The D-dimer levels were>10.000 ng/mL. The EKG was unremarkable. The patient was diagnosed with a NSTEMI.A coronary CTA, which was notable for coronary artery disease. The ECG revealed normal biventricular function or dilated LV, but no wall motion abnormalities. Coronary angiography showed a Spontaneous Coronary Artery Dissection (SCAD) in the D2. SCAD is caused by a tear in one of the epicardial coronary arteries leading to intramural hematoma, compression there to arterial lumen and obstruction to distal coronary flow leading to acute coronary syndrome (ACS). It is a leading cause of ACS in young women, including pregnant and peri-partum women without any cardiovascular risk factors. Pregnancy associated SCAD is the most common cause of pregnancy associated MI accounting to 43% MI in pregnancy. The patient was started on beta blocker and recovered well.

The cardiovascular and hemodynamic changes that occur in pregnancy include the increasing plasma volume from conception to up to 32 weeks. The decrease in the systemic vascular resistance also begins very early after conception. The drop in systemic vascular resistance promotes some sympathetic activity that promotes the tachycardia and the increased heart rate (HR). The stroke volume increases and then plateaued at about 24 weeks. The stroke volume and the increased HR, contribute to the increase in the cardiac output that plateaus at about 24 weeks. There is a 50% increase in the pulmonary blood flow during pregnancy. If the pulmonary vasculature is normal then the vascular resistance decreases. The aorta does not undergo any changes in pregnancy but growth is likely minimal ranging between 1 mm & at the most 10% as measured at the root and the mid-ascending aorta. The left atrial diameter increases by 0.4 centimeter on average. The left ventricular end diastolic diameter increases by 0.3 centimeters as compared to baseline. The LV mass in Normotensive pregnancies increases by about 25 grams. Increase in RV basal & mid diameters. The increasing cardiac output is not necessarily reflected by changes in the ejection fraction. The best way to evaluate the volume changes on the heart during pregnancy is with diastolic studies. In 1st trimester: increase in preload due to initially venoconstriction & later high circulating volumes, lower SVR, increased respiration, E-peak increases more than A-peak. In 2nd trimester: increase in circulating volume, increase in LV mass, LV hypertrophy, A peak increases at about 15 week, E-peak begins to decrease at about 21 weeks E/A decreases, E/e’ increases beginning at around 22 weeks. In 3rd trimester: yet further increase in circulating volumes, further increase in LV mass, LV hypertrophy, E/A decreases, E/e’ increases until 35 weeks, left atrial dilatation. All these return to baseline 6-20 weeks postpartum. There is a reduced ventricular compliance with diastolic dysfunction, but the myocardial function is fine with no damage to the myocardium despite the changes. Hemodynamic changes during labor: increases cardiac output, increase heart rate, increase BP, increase venous return, increase in circulating blood volume with uterine contraction. Effects of the gravid anatomy on TEE consideration: increase in progesterone levels causes decrease in gastric motility and increase in relaxation of the lower esophageal sphincter and increase in intra-abdominal pressure from a gravid uterus. Heightened risk of emesis and aspiration in pregnancy. After 18 weeks gestation, anesthesiologists consider pregnant patient’s fasting status to be “full stomach”. In conclusion, myocardial structural changes during pregnancy are just a response to the normal hemodynamic changes.

Acute coronary syndrome (ACS) complicates 1.7-6.3/100,000 deliveries and pregnancy is associated with a 3-4 fold times increased risk of acute MI acute myocardial infarction (AMI) risk. Coronary artery disease accounts for over 20% of maternal cardiac deaths. In terms of imaging modalities, when a pregnant woman or a woman in her postpartum period presents with ST elevation, MI or elevated troponins, coronary angiogram. In cases which are ambiguous, Intravascular Ultrasound (IVUS) or optical coherence tomography (OCT) is performed. Noninvasive methods such as echocardiography show regional wall motion abnormalities, cardiac MRI with gadolinium for late gadolinium enhancement and coronary angiography with heightened attention to the coronaries as well as myocardial perfusion. IVUS and OCT visualize coronary intima media and adventitia with identification of intramural hematoma. IVUS provides grayscale imaging of the coronary vessel and wall via a catheter with an ultrasound. OCT gives high resolution images, better visualization of internal tears, intra luminal thrombus and hematoma and lumens. While following patients with SCAD, stress echocardiogram, myocardial perfusion imaging or cardiac MRI can be used as they show the extent of ischemia injury and recovery. CT scan and MRI show fibromuscular dysplasia. Routine invasive angiography in asymptomatic patients after SCAD is not recommended. Coronary CT angiography can evaluate both the coronaries as well as myocardial perfusion defects. Major consensus documents recommend arterial imaging from head to pelvis with CT or MRA for evaluating fibromuscular dysplasia or other vascular complications that may need long term follow up.

The 3rd case was a patient G1P1 with a history of gestational hypertension, high obesity (BMI-30), multiple sclerosis, migraines. She presented with 2-month history of progressive orthopnea and recent onset of dyspnea on minimal exertion. On physical examination, she presented mildly hypertensive (143/73 mmHg), tachycardic and with respiratory distress. Regular venous distension, bibasilar crackle, also increased bilateral edema in her legs. Laboratory reports showed elevated D-dimer levels, Troponin-HS and BNP. Cardiomegaly with pulmonary ingestion was seen in Xray. ECG showed an ejection fraction of 15-20%, a severely diluted cavity of 6.3. Diastolic dysfunction and a mildly dilated aorta. She was diagnosed with peripartum cardiomyopathy with acute systolic heart failure exacerbation with NYHA class III. She was initiated with furosemide 20mg IV BID and metoprolol succinate 25 mg OD. On day 3 she was initiated with sacubitril valsartan and day 4 was transitioned to oral furosemide 20mg OD, spironolactone 25mg OD, apixaban 5mg BID and was discharged with a wearable defibrillator. At 1-2 months after discharge, the patient had normal coronaries, she was prescribed losartan as she experienced hypotension with sacubitril valsartan. At 4 months, her EF improved to 36%; apixaban and wearable defibrillator was discontinued.

A case was presented by Dr. Melinda Davis to discuss multimodality imaging approaches to the dyspnoeic pregnant patients. The case was a 32 year old G2P1 at 32 weeks gestation presenting with shortness of breath which was continuously worsening to the level that she could not climb a flight of stairs. The differential diagnosis could be HF with reduced ejection fraction or preserved ejection fraction, pulmonary embolism, valvular heart disease, aortic dissection or ACS. Delays in diagnosis for HF are very common; 25% women are initially misdiagnosed while 52% feel dismissed or an inaccurate diagnosis can lead to delay. Delayed diagnosis is associated with lower EF at diagnosis, less recovery and higher mortality. EKG should be performed in the initial analysis to rule out sinus tachycardia. Chest X-ray which shows pneumonia should be rechecked for HF. Echocardiography is safe to use during pregnancy. Echo contrast may be useful for enhancing imaging quality, to evaluate for intracardiac thrombus and to improve endocardial border definition, wall motion and EF but it has limited data for use in pregnancy. Agitated saline should be avoided during pregnancy. Transesophageal echocardiography has an increased risk of emesis and aspiration. CT with contrast uses ionizing radiation but has a low absolute risk of cancer risk in fetus. Iodinated contrast should be used only when needed and breastfeeding can be continued. Cardiac MRI can be used without contrast and breastfeeding can be continued. In summary, medically necessary imaging should not be withheld during pregnancy.

More than 80% women have 1 child and 1 in 5 live births are complicated by adverse pregnancy outcomes (APs). Data from the Women's Health Initiative shows that AOPs including gestational diabetes, preeclampsia, low birth weight are associated with high risk of Atherosclerotic cardiovascular disease (ASCVD). The trends in age-standardized rates of APOs has demonstrated an increase in the number of hypertensive disorders of pregnancy in the last decade. The trends of age-standardized rates for APOs by race or ethnicity there is a disproportionate low birth and preterm delivery among hypertensive disorders of pregnancy among Hispanic White, non-Hispanic black, Hispanic and Asians. In pregnancies, complicated with preeclampsia, there is endothelial dysfunction and vasoconstriction leading to constricted lefty ventricular hypertrophy which is less likely to recover postpartum. The cardiac impairments in late pregnancy in severe preeclampsia can lead to increased LV wall thickness, abnormal RV strain, diastolic dysfunction, increased RV systolic pressure and left atrial enlargement. There can also be higher rates of grade II diastolic function and peripartum pulmonary edema. In early postpartum, where there is incidence of persistent cardiac impairment, at 1 year there can be a higher rate of left ventricular moderate-severe dysfunction/hypertrophy in preterm preeclampsia as compared with term preeclampsia (P<0/001). In data from studies on women in 10 years postpartum period, show that most of these women have a four-fold risk of developing hypertension. They even have higher interventricular septal wall thickness, higher LV remodeling and lower mitral inflow. A Swedish study has shown that there is a 32.1% prevalence of any coronary atherosclerosis in women with a history of any APO. Results from the Copenhagen Preeclampsia and Cardiovascular Disease (CPH-PRECIOUS) study demonstrated an increase in the odds ratio of developing coronary atherosclerosis are higher in women with history preeclampsia as compared to women without prior preeclampsia. Women with a history of gestational diabetes have a two-fold increased risk of calcium score across all levels of glucose tolerance. Other vascular structure and vascular function abnormalities include increased carotid intima media thickness, increased retinal microvascular, low flow mediated dilation, low peripheral arterial tonometry, and increased pulse wave velocity. In conclusion, the cardiovascular implications of APOs can occur after the birth of the infant. Calcium score and CCTA are useful tools to risk stratify women with APOs.

American College of Cardiology (ACC) International Congress 2023, 4th March - 6th March 2023, New Orleans